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p(FPLX:CHRN)

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Entity

Name
CHRN
Namespace
FPLX
Namespace Version
20180917
Namespace URL
https://raw.githubusercontent.com/sorgerlab/famplex/e8ae9926ff95266032cb74f77973c84939bffbeb/export/famplex.belns

Appears in Networks 11

Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System v1.0.0

Neuronal Nicotinic Acetylcholine Receptor Structure and Function and Response to Nicotine v1.0.1

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0

NACHO Mediates Nicotinic Acetylcholine Receptor Function throughout the Brain v1.0.0

Neural Systems Governed by Nicotinic Acetylcholine Receptors: Emerging Hypotheses v1.0.0

Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0

Chaperoning α7 neuronal nicotinic acetylcholine receptors v1.0.0

Naturally-expressed nicotinic acetylcholine receptor subtypes v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

In-Edges 143

complex(a(CHEBI:epibatidine), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

a(CHEBI:genistein) regulates p(FPLX:CHRN) View Subject | View Object

Results show that genistein does not alter the surface expression of nAChRs, but rather it modifies nAChRs in the cell membrane (71). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Cell Membrane

a(CHEBI:acetylcholine) increases act(p(FPLX:CHRN)) View Subject | View Object

We now realize that acetylcholine liberated from cholinergic nerve terminals often activates both nAChRs and muscarinic receptors PubMed:21482353

Appears in Networks:

a(CHEBI:nicotine) increases act(p(FPLX:CHRN)) View Subject | View Object

Activation and desensitization of nAChRs by bath-applied nicotine also increases LTD induced by a stimulus train PubMed:17009926

Appears in Networks:

a(CHEBI:nicotine) increases p(FPLX:CHRN) View Subject | View Object

This puzzle does not yet have a complete answer, but it is clear that chronic nicotine increases the number of nAChRs themselves (Marks et al., 1983; Schwartz and Kellar, 1983) PubMed:21482353

Appears in Networks:

complex(a(HBP:"alpha-Bungarotoxin"), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:RIC3)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") increases act(p(FPLX:CHRN)) View Subject | View Object

The most commonly prescribed treatments for AD are acetylcholinesterase inhibitors, which decrease the hydrolysis rate of ACh and, thereby, enhance cholinergic signaling. One such drug, galantamine (Reminyl), also potentiates nAChRs (66). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:choline) increases act(p(FPLX:CHRN)) View Subject | View Object

Another important aspect of this diffusive ACh signal is that its eventual hydrolysis creates choline, which also activates and desensitizes nAChRs in a subtype-selective manner (54, 55). PubMed:17009926

Appears in Networks:

a(CHEBI:galanthamine) increases act(p(FPLX:CHRN)) View Subject | View Object

The most commonly prescribed treatments for AD are acetylcholinesterase inhibitors, which decrease the hydrolysis rate of ACh and, thereby, enhance cholinergic signaling. One such drug, galantamine (Reminyl), also potentiates nAChRs (66). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:genistein) causesNoChange surf(p(FPLX:CHRN)) View Subject | View Object

Results show that genistein does not alter the surface expression of nAChRs, but rather it modifies nAChRs in the cell membrane (71). PubMed:17009926

Appears in Networks:

a(CHEBI:nicotine) increases act(p(FPLX:CHRN)) View Subject | View Object

The nicotine initially activates nAChRs on DA neurons, causing an increase in burst firing and overall firing rate (88, 121, 123, 124, 134). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
dopaminergic neuron

bp(GO:"developmental process") association p(FPLX:CHRN) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

bp(GO:"regulation of action potential firing pattern") association p(FPLX:CHRN) View Subject | View Object

Acting through these excitatory and inhibitory inputs and nAChRs located on the DA neurons, nicotinic receptors influence the firing modes and firing frequency of DA neurons (119, 121). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
midbrain dopaminergic neuron
MeSH
Dendrites
MeSH
Neocortex

bp(GO:"regulation of action potential firing rate") association p(FPLX:CHRN) View Subject | View Object

Acting through these excitatory and inhibitory inputs and nAChRs located on the DA neurons, nicotinic receptors influence the firing modes and firing frequency of DA neurons (119, 121). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
midbrain dopaminergic neuron
MeSH
Dendrites
MeSH
Neocortex

bp(GO:"regulation of synaptic plasticity") association p(FPLX:CHRN) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

bp(GO:"regulation of synaptic plasticity") association p(FPLX:CHRN) View Subject | View Object

Nicotinic receptors also modulate glutamatergic synaptic plasticity. PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
glutamatergic neuron

bp(GO:"response to pain") association p(FPLX:CHRN) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

bp(GO:learning) association p(FPLX:CHRN) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

bp(GO:memory) association p(FPLX:CHRN) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

composite(a(CHEBI:acetylcholine), a(CHEBI:ivermectin)) increases act(p(FPLX:CHRN)) View Subject | View Object

For example, ivermectin increases the apparent ACh affinity, the slope of the dose-response curve, and the amplitude of nAChR responses (68). PubMed:17009926

Appears in Networks:

path(MESH:Epilepsy) association p(FPLX:CHRN) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

path(MESH:"Alzheimer Disease") association p(FPLX:CHRN) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

As AD worsens, cholinergic neurons are progressively lost and the number of nAChRs declines, particularly in the hippocampus and cortex (140, 158). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
cholinergic neuron
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

path(MESH:"Autistic Disorder") association p(FPLX:CHRN) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

path(MESH:"Autistic Disorder") negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Autistic Disorder") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Behavior, Addictive") association p(FPLX:CHRN) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

path(MESH:"Down Syndrome") negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Down Syndrome") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Lewy Body Disease") negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Lewy Body Disease") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Parkinson Disease") negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:"Parkinson Disease") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

path(MESH:Anxiety) association p(FPLX:CHRN) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

path(MESH:Attention) association p(FPLX:CHRN) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

path(MESH:Depression) association p(FPLX:CHRN) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

path(MESH:Epilepsy) association p(FPLX:CHRN) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

path(MESH:Schizophrenia) association p(FPLX:CHRN) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

path(MESH:Schizophrenia) association p(FPLX:CHRN) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

a(CHEBI:"calcium(2+)") regulates act(p(FPLX:CHRN)) View Subject | View Object

Although calcium modulation can act intracellularly, nAChRs also are allosterically modulated by extracellular calcium, leading to dramatic changes in the channel opening probability (Amador & Dani, 1995; Mulle, Lena, & Changeux, 1992; Vernino et al., 1992). PubMed:26472524

Appears in Networks:
Annotations
MeSH
Extracellular Space

a(CHEBI:"calcium(2+)") regulates p(FPLX:CHRN) View Subject | View Object

Moreover,nicotinic receptors can also be regulated allosterically by Ca2+ PubMed:26813123

Appears in Networks:

a(CHEBI:acetylcholine) increases act(p(FPLX:CHRN)) View Subject | View Object

When cholinergic neurons are depolarized, ACh is exocytosed from synaptic vesicles and released into the synaptic cleft, where it can activate both muscarinic and nicotinic receptors PubMed:26813123

Appears in Networks:

a(CHEBI:tubocurarine) decreases act(p(FPLX:CHRN)) View Subject | View Object

Curare is the best known antagonist for nicotinic receptors, although this drug is not capable of blocking central nicotinic receptors PubMed:26813123

Appears in Networks:

complex(a(CHEBI:"1,1-dimethyl-4-phenylpiperazinium iodide"), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"1,1-dimethyl-4-phenylpiperazinium iodide"), p(FPLX:CHRN)) increases act(p(FPLX:CHRN)) View Subject | View Object

Not only nicotine, but also DMPP (1,1-Dimethyl-4- phenylpiperazinium) and cystine can act as nicotinic receptor agonists PubMed:26813123

Appears in Networks:

complex(a(CHEBI:cystine), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:cystine), p(FPLX:CHRN)) increases act(p(FPLX:CHRN)) View Subject | View Object

Not only nicotine, but also DMPP (1,1-Dimethyl-4- phenylpiperazinium) and cystine can act as nicotinic receptor agonists PubMed:26813123

Appears in Networks:

complex(a(CHEBI:nicotine), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:nicotine), p(FPLX:CHRN)) increases act(p(FPLX:CHRN)) View Subject | View Object

Not only nicotine, but also DMPP (1,1-Dimethyl-4- phenylpiperazinium) and cystine can act as nicotinic receptor agonists PubMed:26813123

Appears in Networks:

complex(p(HGNC:CHRNA1), p(HGNC:CHRNA1), p(HGNC:CHRNB1), p(HGNC:CHRND), p(HGNC:CHRNG)) increases p(FPLX:CHRN) View Subject | View Object

Cholinergic nicotinic receptors expressed in muscle and ganglia are comprised of two α subunits plus each of the other three PubMed:26813123

Appears in Networks:
Annotations
MeSH
Ganglia
MeSH
Muscles

p(FPLX:CHRN, pmod(Ph)) regulates act(p(FPLX:CHRN)) View Subject | View Object

It has been demonstrated that phosphorylation of nicotinic receptors by protein kinase A, protein kinase C, and tyrosine kinase can regulate receptor activity PubMed:26813123

Appears in Networks:

p(MGI:App, var("?")) decreases p(FPLX:CHRN) View Subject | View Object

In addition, quantitative autoradiography assay revealed that choline uptake was reduced in the hippocampus of these animals and that the expression of muscarinic and nicotinic cholinergic receptors was diminished PubMed:26813123

Appears in Networks:
Annotations
MeSH
Hippocampus

a(CHEBI:"amyloid-beta polypeptide 42") decreases act(p(FPLX:CHRN)) View Subject | View Object

With the use of selective antagonists it was possible to determine that inhibition operates on both alpha7 and non-alpha7 receptors (Pettit et al., 2001) PubMed:25514383

Appears in Networks:

a(CHEBI:"amyloid-beta polypeptide 42") decreases act(p(FPLX:CHRN)) View Subject | View Object

They demonstrated that Abeta1-42 drives a reversible inhibition of nAChR-mediated currents in hippocampal GABAergic neurons recorded from rat slices. In these experimental conditions the most effective Abeta1-42 concentration was 500 nM, but inhibition was found also at the lower concentration of 100 nM PubMed:25514383

Appears in Networks:
Annotations
Cell Ontology (CL)
GABAergic neuron
MeSH
Hippocampus

a(CHEBI:"amyloid-beta") regulates act(p(FPLX:CHRN)) View Subject | View Object

Modulation of nAChRs by Abeta was also found in ex vivo studies: Pettit and colleagues (2001) used rat hippocampal slices to show that Abeta1-42 incubation is able to reduce postsynaptic currents and open probability of both alpha7 and non-alpha7 nAChRs subtypes, demonstrating an interaction between Abeta and other nAChR subunits PubMed:25514383

Appears in Networks:

a(CHEBI:"amyloid-beta") decreases act(p(FPLX:CHRN)) View Subject | View Object

It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383

Appears in Networks:

a(MESH:"Cysteine Loop Ligand-Gated Ion Channel Receptors") hasMember p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN), p(HGNC:FLNA)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:acetylcholine), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

path(MESH:"Alzheimer Disease") decreases p(FPLX:CHRN) View Subject | View Object

Binding studies performed with the use of [3H]-nicotine and [3H]-ACh showed a significant reduction in nicotine and ACh binding sites in cerebral cortex of patients suffering from AD, demonstrating a decrease of both nAChR and mAChR populations (Gotti et al., 2006a; Paterson and Nordberg, 2000; Perry et al., 1981, 1985, 1987, 1988; Shimohama et al., 1986; Whitehouse et al., 1981, 1982, 1986) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

a(CHEBI:nicotine) regulates p(FPLX:CHRN) View Subject | View Object

nAChRs also underlie the behavioral and addictive properties of nicotine PubMed:28445721

Appears in Networks:

act(a(GO:synapse)) regulates p(FPLX:CHRN) View Subject | View Object

At the cellular level, nAChRs can underlie synaptic responses, neuronal excitability, and neurotransmitter release (Dajas-Bailador and Wonnacott, 2004; Gotti and Clementi, 2004; Hogg et al., 2003) PubMed:28445721

Appears in Networks:

bp(GO:"neuronal action potential") regulates p(FPLX:CHRN) View Subject | View Object

At the cellular level, nAChRs can underlie synaptic responses, neuronal excitability, and neurotransmitter release (Dajas-Bailador and Wonnacott, 2004; Gotti and Clementi, 2004; Hogg et al., 2003) PubMed:28445721

Appears in Networks:

bp(GO:"neurotransmitter secretion") regulates p(FPLX:CHRN) View Subject | View Object

At the cellular level, nAChRs can underlie synaptic responses, neuronal excitability, and neurotransmitter release (Dajas-Bailador and Wonnacott, 2004; Gotti and Clementi, 2004; Hogg et al., 2003) PubMed:28445721

Appears in Networks:

bp(GO:cognition) association p(FPLX:CHRN) View Subject | View Object

As ACh-gated cation channels, these broadly distributed receptors participate in arousal, motivation, and numerous aspects of cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996). PubMed:28445721

Appears in Networks:

bp(GO:cognition) association p(FPLX:CHRN) View Subject | View Object

Because nAChRs play important roles in cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996), we focused attention on this behavi PubMed:28445721

Appears in Networks:

complex(a(MESH:Bungarotoxins), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

Resistance to inhibitor of cholinesterase-3 (RIC-3) is required for nAChR function in C. elegans (Nguyen et al., 1995) PubMed:28445721

Appears in Networks:

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

Whereas RIC-3 can enhance function of certain mammalian nAChRs, RIC-3 is not essential (Koperniak et al., 2013) PubMed:28445721

Appears in Networks:

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

In C. elegans, RIC-3 protein is essential for nAChR function (Nguyen et al., 1995), and mammalian RIC-3 has modest and mixed effects on nAChRs (Halevi et al., 2003; Millar, 2008) PubMed:28445721

Appears in Networks:

p(MGI:Tmem35a) regulates p(FPLX:CHRN) View Subject | View Object

A very recent study also reported memory defects in mice lacking NACHO/TMEM35 done by scientists unaware of NACHO’s role in controlling nAChRs (Kennedy et al., 2016) PubMed:28445721

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p(MGI:Tmem35a) increases p(FPLX:CHRN) View Subject | View Object

In membranes from cerebral cortex, hippocampus, and striatum, we found that levels of [3H]epibatidine binding sites are decreased by 50%–75% PubMed:28445721

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Corpus Striatum
MeSH
Hippocampus

path(MESH:"Tobacco Use Disorder") association p(FPLX:CHRN) View Subject | View Object

Indeed, presynaptic effects of nAChRs in regulating dopamine release in basal ganglia and prefrontal cortex likely participate in nicotine’s addictive and cognitive effects, respectively (Jasinska et al., 2014) PubMed:28445721

Appears in Networks:

path(MESH:Arousal) association p(FPLX:CHRN) View Subject | View Object

As ACh-gated cation channels, these broadly distributed receptors participate in arousal, motivation, and numerous aspects of cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996). PubMed:28445721

Appears in Networks:

path(MESH:Motivation) association p(FPLX:CHRN) View Subject | View Object

As ACh-gated cation channels, these broadly distributed receptors participate in arousal, motivation, and numerous aspects of cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996). PubMed:28445721

Appears in Networks:

a(CHEBI:nicotine) increases act(p(FPLX:CHRN)) View Subject | View Object

Nicotine both activates and desensitizes nAChRs in midbrain dopaminergic neurons (Brodie, 1991; Pidoplichko et al., 1997), and the pleasurable effects associated with nicotine intake occur in large part via the mesolimbic dopaminergic reward system (Corrigall et al., 1992; Koob and Volkow,2010) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:nicotine) increases p(FPLX:CHRN) View Subject | View Object

At the level of whole brain, chronic nicotine causes selective upregulation of nAChRs among major brain regions. Upregulation occurs in cortex, midbrain, and hypothalamus, but not in thalamus or cerebellum (Pauly et al., 1991; Marks et al., 1992; Nguyen et al., 2003; Nashmi et al., 2007; Doura et al., 2008) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hypothalamus
MeSH
Mesencephalon

a(CHEBI:nicotine) causesNoChange p(FPLX:CHRN) View Subject | View Object

At the level of whole brain, chronic nicotine causes selective upregulation of nAChRs among major brain regions. Upregulation occurs in cortex, midbrain, and hypothalamus, but not in thalamus or cerebellum (Pauly et al., 1991; Marks et al., 1992; Nguyen et al., 2003; Nashmi et al., 2007; Doura et al., 2008) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Cerebellum
MeSH
Thalamus

act(a(MESH:Brain)) negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Because excess activation of nAChRs damages neuronal health and brain function, organisms have a clear need to restrict the degree of nAChR activation PubMed:21482353

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a(MESH:Neurons) negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Because excess activation of nAChRs damages neuronal health and brain function, organisms have a clear need to restrict the degree of nAChR activation PubMed:21482353

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p(HGNC:LYNX1) regulates act(p(FPLX:CHRN)) View Subject | View Object

Therefore, the evolutionary relationship between lynx modulators and the alpha-neurotoxins agrees with the view that lynx modulators govern critical control points in the pathway of nicotinic receptor signaling PubMed:21482353

Appears in Networks:

p(HGNC:LYNX1) decreases act(p(FPLX:CHRN)) View Subject | View Object

Lynx1, the first discovered member of this family expressed in the brain (Miwa et al., 1999), has an overall inhibitory effect on nAChR function PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:LYNX1) decreases act(p(FPLX:CHRN)) View Subject | View Object

Removal of the molecular brake provided by lynx proteins can lead to nicotinic receptor hypersensitivity—larger direct nicotinic responses, slowed desensitization kinetics (Miwa et al., 2006), and enhanced sensitivity of the EPSC frequency in the cortex to nicotine (Tekinay et al., 2009) PubMed:21482353

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p(HGNC:LYNX1) regulates act(p(FPLX:CHRN)) View Subject | View Object

This indicates that lynx proteins exist, genetically, as upstream modulators of nicotinic receptor function and cholinergic signaling and can exert control over cholinergic-dependent processes PubMed:21482353

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complex(a(INTERPRO:"14-3-3 protein"), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(INTERPRO:"14-3-3 protein"), p(FPLX:CHRN)) increases p(FPLX:CHRN) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(a(INTERPRO:"14-3-3 protein"), p(FPLX:CHRN)) increases act(p(FPLX:CHRN)) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(p(FPLX:CHRN), p(HGNC:LYNX1)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:LYNX1)) regulates act(p(FPLX:CHRN)) View Subject | View Object

Proteins that engage nAChRs within stable complexes, such as lynx family members, provide a homeostatic influence over nicotinic receptor systems PubMed:21482353

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:LYNX1)) association act(p(FPLX:CHRN)) View Subject | View Object

As GPI-anchored proteins can bind to transmembrane receptors intracellularly, the interactions of lynx with nAChRs could potentially alter receptor trafficking, stoichiometry, and surface number (Lester et al., 2009) PubMed:21482353

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:LYNX1)) association surf(p(FPLX:CHRN)) View Subject | View Object

As GPI-anchored proteins can bind to transmembrane receptors intracellularly, the interactions of lynx with nAChRs could potentially alter receptor trafficking, stoichiometry, and surface number (Lester et al., 2009) PubMed:21482353

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:RIC3)) increases p(FPLX:CHRN) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(p(FPLX:CHRN), p(HGNC:RIC3)) increases act(p(FPLX:CHRN)) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(p(FPLX:CHRN), p(HGNC:VSNL1)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:VSNL1)) increases p(FPLX:CHRN) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(p(FPLX:CHRN), p(HGNC:VSNL1)) increases act(p(FPLX:CHRN)) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(p(FPLX:CHRN), p(INTERPRO:Neurexin)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(p(FPLX:CHRN), p(INTERPRO:Neurexin)) increases p(FPLX:CHRN) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

complex(p(FPLX:CHRN), p(INTERPRO:Neurexin)) increases act(p(FPLX:CHRN)) View Subject | View Object

Finally, nAChRs exist in complexes in the brain; interacting proteins engage in complexes with nAChRs and aid in the assembly and trafficking of nAChR to the plasma membrane; examples are RIC-3 (Lansdell et al., 2005), 14-3-3 proteins (Jeanclos et al., 2001), neurexins (Cheng et al., 2009), and VILIP-1 (Lin et al., 2002) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

composite(a(HBP:"alpha-4 beta-2 nAChR"), p(HGNC:LYNX1)) decreases act(p(FPLX:CHRN)) View Subject | View Object

In an alpha4beta2* nAChR-expressing cell, coexpression of lynx1 results in reduced agonist sensitivity, accelerated onset of desensitization, and slower recovery from desensitization (Ibanez-Tallon et al., 2002) PubMed:21482353

Appears in Networks:

path(MESH:Schizophrenia) association act(p(FPLX:CHRN)) View Subject | View Object

Recent studies provide evidence both that nicotinic signaling partially underlies these schizophrenia-related inhibitory defects and that nicotinic drugs have possible therapeutic roles PubMed:21482353

Appears in Networks:

path(MESH:"Tobacco Use Disorder") association act(p(FPLX:CHRN)) View Subject | View Object

Developmental changes in nAChR functions may play a role in nicotine addiction, as a central question in tobacco control is young adult smokers’ marked sensitivity to developing nicotine dependence (DSM-V Nicotine Workgroup, 2010; DiFranza et al., 2000; Difranza, 2010) PubMed:21482353

Appears in Networks:

a(MESH:"Amyloid beta-Peptides") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

a(CHEBI:Ondansetron) decreases p(FPLX:CHRN) View Subject | View Object

Nerve growth factor intraventricularly administered to AD patients for 3 months resulted in an increased [11C]nicotine binding (Eriksdotter-Jo¨nhagen et al 1998), whereas treatment with the 5-HT3 blocker ondansetron showed a decreased number of cortical nAChRs (Nordberg et al 1997) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

a(CHEBI:tacrine) increases p(FPLX:CHRN) View Subject | View Object

In addition, PET studies also have revealed an improvement in nAChRs in AD patients during long-term treatment with cholinesterase inhibitors such as tacrine and NXX- 066 (Nordberg 2000; Nordberg et al 1992, 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(UNIPROT:P34371) increases act(p(FPLX:CHRN)) View Subject | View Object

Reduced expression of the lat- ter protein has been shown to be detrimental to AChR function in C. elegans [113] (See Fig. 2). PubMed:22040696

Appears in Networks:

a(MESH:"Neurotransmitter Agents") association p(FPLX:CHRN) View Subject | View Object

Experimental data suggest that the nAChRs might act as neuromodulators in communicative processes in the brain (Kaiser et al 2000; Lindstro¨m 1997; Wonnacott 1997) PubMed:11230871

Appears in Networks:

a(PUBCHEM:132228) increases p(FPLX:CHRN) View Subject | View Object

In addition, PET studies also have revealed an improvement in nAChRs in AD patients during long-term treatment with cholinesterase inhibitors such as tacrine and NXX- 066 (Nordberg 2000; Nordberg et al 1992, 1998) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"response to oxidative stress") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

bp(GO:cognition) association p(FPLX:CHRN) View Subject | View Object

Interestingly enough, a considerable body of evidence exists to suggest that the nAChRs are involved in cognitive and memory functions (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Sahakian and Coull 1994) PubMed:11230871

Appears in Networks:

bp(GO:memory) association p(FPLX:CHRN) View Subject | View Object

Interestingly enough, a considerable body of evidence exists to suggest that the nAChRs are involved in cognitive and memory functions (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Sahakian and Coull 1994) PubMed:11230871

Appears in Networks:

bp(MESH:"Lipid Peroxidation") decreases p(FPLX:CHRN) View Subject | View Object

Interestingly enough, lipid peroxidation has been shown to decrease the number of nAChRs in PC12 cells (Guan et al 2000a) PubMed:11230871

Appears in Networks:

complex(a(CHEBI:cytisine), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

p(HGNC:APP, var("p.Lys670Asn"), var("p.Met671Leu")) negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Significant reductions in the number of nAChRs were measured in cortical regions of Swedish APP 670/ 671 mutation (273% to 287%) (Marutle et al 1999) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

path(MESH:"Alzheimer Disease") association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

path(MESH:"Alzheimer Disease") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

A consistent, significant loss of nAChRs has been observed in cortical autopsy brain tissue from AD patients relative to age-matched healthy subjects (Nordberg and Winblad 1986) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

path(MESH:"Cognitive Dysfunction") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

The cortical nAChR deficits significantly correlate with cognitive impairment in AD patients (Nordberg, in press; Nordberg et al 1995, 1997) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

path(MESH:"Parkinson Disease") association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

path(MESH:"Tourette Syndrome") association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

path(MESH:Anxiety) association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

path(MESH:Depression) association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

path(MESH:Epilepsy) association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

path(MESH:Schizophrenia) association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

a(CHEBI:nicotine) increases act(p(FPLX:CHRN)) View Subject | View Object

In terms of functional effects, nicotine acts acutely much in the way that ACh does, causing opening of nAChR channels. PubMed:21787755

Appears in Networks:

bp(GO:"phosphatidylinositol 3-kinase signaling") increases p(FPLX:CHRN) View Subject | View Object

Recent studies have also demonstrated the importance of the phos- phatidylinositol 3-kinase (PI3K) pathway downstream of AChRs in pro- tecting neurons from death and up-regulating these receptors [148]. PubMed:22040696

Appears in Networks:

complex(GO:"proteasome complex") regulates p(FPLX:CHRN) View Subject | View Object

Regulation of receptor subunits by the proteasome, the large pro- tein complex that proteolytically degrades unneeded proteins, has also been demonstrated [113,114]. PubMed:22040696

Appears in Networks:

complex(p(FPLX:CHRN), p(FPLX:SRC)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(p(FPLX:CHRN), p(HGNC:FYN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

act(p(HGNC:RIC3), ma(chap)) increases p(FPLX:CHRN) View Subject | View Object

More re- cently, the transmembrane protein resistant to inhibitors of cholines- terase (RIC-3), originally identified in Caenorhabditis elegans, has been classed as a much more selective chaperone of the AChR [71,107–112]. PubMed:22040696

Appears in Networks:

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

Co-expression with RIC-3 was shown to be required for AChR ac- tivity in C. elegans body muscles and for enhanced AChR activity in Xenopus oocytes [110,112]. PubMed:22040696

Appears in Networks:

act(p(HGNC:RIC3), ma(chap)) increases p(FPLX:CHRN) View Subject | View Object

Interestingly, levels of RIC-3 mRNA are elevat- ed in postmortem brains of individuals with bipolar disorder and schizophrenia [181], and a link has been suggested between defi- cient RIC-3 mediated chaperoning of an AChR subunit and individ- uals with bipolar disorder and psychotic symptoms [181]. PubMed:22040696

Appears in Networks:
Annotations
MeSH
Brain

p(FPLX:"p14_3_3") increases p(FPLX:CHRN) View Subject | View Object

There is evidence that AChR folding, assembly and trafficking are influenced by several chaperone proteins, such as the 14-3-3 protein [92,93], BiP [94–96] or calnexin [97–99]. PubMed:22040696

Appears in Networks:

p(FPLX:CHRN, pmod(Ph, Tyr)) decreases act(p(FPLX:CHRN)) View Subject | View Object

In Torpedo electric organ, phosphorylation of AChRs by SFKs causes subtle changes in desensitization kinetics but not in I max , the maximal current flowing through the receptor channel [141–143]. PubMed:22040696

Appears in Networks:

p(HGNC:CANX) increases p(FPLX:CHRN) View Subject | View Object

There is evidence that AChR folding, assembly and trafficking are influenced by several chaperone proteins, such as the 14-3-3 protein [92,93], BiP [94–96] or calnexin [97–99]. PubMed:22040696

Appears in Networks:

p(HGNC:HSPA5) increases p(FPLX:CHRN) View Subject | View Object

There is evidence that AChR folding, assembly and trafficking are influenced by several chaperone proteins, such as the 14-3-3 protein [92,93], BiP [94–96] or calnexin [97–99]. PubMed:22040696

Appears in Networks:

a(CHEBI:acetylcholine) increases act(p(FPLX:CHRN)) View Subject | View Object

In terms of functional effects, nicotine acts acutely much in the way that ACh does, causing opening of nAChR channels. PubMed:21787755

Appears in Networks:

complex(a(CHEBI:galanthamine), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:galanthamine), p(FPLX:CHRN)) increases act(p(FPLX:CHRN)) View Subject | View Object

Besides, galantamine allosterically interacted with nicotinic ACh receptors to increase the agonistic activity of these receptors and amplified the ACh reaction through stimulating ACh release [165–167]. PubMed:29179999

Appears in Networks:

Out-Edges 129

p(FPLX:CHRN) increases bp(GO:cognition) View Subject | View Object

Agonists of nicotinic ACh receptors can improve, while antagonists for the receptor impair, performance in cognitive tasks PubMed:26813123

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Epilepsy) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Anxiety) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases bp(GO:"maintenance of synapse structure") View Subject | View Object

Moreover, some nAChRs have been implicated in processes such as the structuring and maintenance of neurites and synapses [18–20] and even in modulation of neuronal viability/death [21–24]. PubMed:21787755

Appears in Networks:

p(FPLX:CHRN) increases bp(GO:"neuron projection maintenance") View Subject | View Object

Moreover, some nAChRs have been implicated in processes such as the structuring and maintenance of neurites and synapses [18–20] and even in modulation of neuronal viability/death [21–24]. PubMed:21787755

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Depression) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases bp(GO:"neurotransmitter secretion") View Subject | View Object

Presynaptic and preterminal nicotinic receptors enhance neurotransmitter release, and postsynaptic and nonsynaptic nAChRs mediate excitation as well as activity-dependent modulation of circuits and intracellular enzymatic processes. PubMed:17009926

Appears in Networks:
Annotations
MeSH
Presynaptic Terminals

act(p(FPLX:CHRN)) increases bp(GO:"neurotransmitter secretion") View Subject | View Object

Activation of presynaptic nAChRs increases the release of many different neurotransmitters (1, 2, 4, 5, 40, 41, 77–83). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Presynaptic Terminals

p(FPLX:CHRN) increases bp(GO:"neurotransmitter secretion") View Subject | View Object

Presynaptic and preterminal nAChRs increase the release of neurotransmitters in the hippocampus, particularly the main neurotransmitters, GABA and glutamate (41, 78, 81, 97). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Presynaptic Terminals

p(FPLX:CHRN) regulates bp(GO:"rhythmic excitation") View Subject | View Object

Presynaptic and preterminal nicotinic receptors enhance neurotransmitter release, and postsynaptic and nonsynaptic nAChRs mediate excitation as well as activity-dependent modulation of circuits and intracellular enzymatic processes. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) regulates bp(GO:"rhythmic excitation") View Subject | View Object

Furthermore, by directly exciting or by shunting the progress of an action potential at a bifurcation, axonal or dendritic nAChRs alter the spread of neuronal excitation. PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
neuron
MeSH
Axons
MeSH
Dendrites

p(FPLX:CHRN) regulates bp(GO:"neuron remodeling") View Subject | View Object

Presynaptic and preterminal nicotinic receptors enhance neurotransmitter release, and postsynaptic and nonsynaptic nAChRs mediate excitation as well as activity-dependent modulation of circuits and intracellular enzymatic processes. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association bp(GO:"regulation of synaptic plasticity") View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(GO:"regulation of synaptic plasticity") View Subject | View Object

Nicotinic stimulation enhances glutamate release on multiple timescales, extending from seconds to a few minutes (81), and contributes to the induction of synaptic plasticity (4, 13, 14, 16, 88). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association bp(GO:"regulation of synaptic plasticity") View Subject | View Object

Nicotinic receptors also modulate glutamatergic synaptic plasticity. PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
glutamatergic neuron

p(FPLX:CHRN) association path(MESH:Attention) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association bp(GO:learning) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association bp(GO:memory) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association bp(GO:"developmental process") View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Schizophrenia) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Schizophrenia) View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Epilepsy) View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association path(MESH:"Autistic Disorder") View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) negativeCorrelation path(MESH:"Autistic Disorder") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Autistic Disorder") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association path(MESH:"Alzheimer Disease") View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

As AD worsens, cholinergic neurons are progressively lost and the number of nAChRs declines, particularly in the hippocampus and cortex (140, 158). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
cholinergic neuron
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(FPLX:CHRN) association path(MESH:"Behavior, Addictive") View Subject | View Object

Decline, disruption, or alterations of nicotinic cholinergic mechanisms have been implicated in various dysfunctions, such as schizophrenia, epilepsy, autism, Alzheimer’s disease (AD), and addiction (17–23). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Monovalent"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Monovalent"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Divalent"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations. PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Divalent"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations. PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

Nicotinic receptor activity causes depolarization, and the divalent cation perme- ability plays an important physiological role by supplying ionic signals, including calcium (39–41). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

In addition, nAChR activity produces a depolarization that activates voltage-gated calcium channels in the presynaptic terminal (87). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Presynaptic Terminals

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

Activation of nAChRs on distal apical dendrites depolarizes the cell and promotes action potential firing PubMed:17009926

Appears in Networks:
Annotations
MeSH
Dendrites
MeSH
Neocortex

act(p(FPLX:CHRN)) increases tloc(a(CHEBI:"calcium(2+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

Nicotinic receptors mediate a small direct calcium influx (42–44, 85). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Nicotinic stimulation enhances glutamate release on multiple timescales, extending from seconds to a few minutes (81), and contributes to the induction of synaptic plasticity (4, 13, 14, 16, 88). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Presynaptic and preterminal nAChRs increase the release of neurotransmitters in the hippocampus, particularly the main neurotransmitters, GABA and glutamate (41, 78, 81, 97). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Presynaptic Terminals

p(FPLX:CHRN) increases sec(a(CHEBI:"gamma-aminobutyric acid")) View Subject | View Object

Presynaptic and preterminal nAChRs increase the release of neurotransmitters in the hippocampus, particularly the main neurotransmitters, GABA and glutamate (41, 78, 81, 97). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Presynaptic Terminals

p(FPLX:CHRN) regulates act(complex(GO:"GABA-A receptor complex")) View Subject | View Object

In the rat CA3 region, spontaneous activation of GABA A receptors produces giant depolarizing potentials, whose frequency is controlled by α7∗ and non-α7 nAChRs. PubMed:17009926

Appears in Networks:
Annotations
MeSH
CA3 Region, Hippocampal

act(p(FPLX:CHRN)) increases bp(GO:"long term synaptic depression") View Subject | View Object

Activation and desensitization of nAChRs by bath-applied nicotine also increases LTD induced by a stimulus train PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(GO:"regulation of action potential firing rate") View Subject | View Object

Activation of nAChRs on distal apical dendrites depolarizes the cell and promotes action potential firing PubMed:17009926

Appears in Networks:
Annotations
MeSH
Dendrites
MeSH
Neocortex

p(FPLX:CHRN) association bp(GO:"regulation of action potential firing rate") View Subject | View Object

Acting through these excitatory and inhibitory inputs and nAChRs located on the DA neurons, nicotinic receptors influence the firing modes and firing frequency of DA neurons (119, 121). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
midbrain dopaminergic neuron
MeSH
Dendrites
MeSH
Neocortex

p(FPLX:CHRN) increases bp(GO:"regulation of action potential firing rate") View Subject | View Object

The nicotine initially activates nAChRs on DA neurons, causing an increase in burst firing and overall firing rate (88, 121, 123, 124, 134). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
dopaminergic neuron

p(FPLX:CHRN) association bp(GO:"regulation of action potential firing pattern") View Subject | View Object

Acting through these excitatory and inhibitory inputs and nAChRs located on the DA neurons, nicotinic receptors influence the firing modes and firing frequency of DA neurons (119, 121). PubMed:17009926

Appears in Networks:
Annotations
Cell Ontology (CL)
midbrain dopaminergic neuron
MeSH
Dendrites
MeSH
Neocortex

act(p(FPLX:CHRN)) negativeCorrelation path(MESH:"Lewy Body Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Lewy Body Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) negativeCorrelation path(MESH:"Down Syndrome") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Down Syndrome") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

Appears in Networks:

p(FPLX:CHRN) association bp(GO:"response to pain") View Subject | View Object

Genetic evidence has linked nicotinic receptors to epilepsy and schizophrenia, and studies with mutant mice have implicated nAChRs in pain mechanisms, anxiety, and depression. PubMed:17009926

Appears in Networks:

act(p(FPLX:CHRN)) increases path(MESH:Arousal) View Subject | View Object

Moreover, although nicotine increases wakefulness in wild-type mice, it does not affect β2−/− mice. Overall, stimulation of nAChRs promotes arousal and REM sleep. PubMed:17009926

Appears in Networks:
Annotations
MeSH
Epilepsy

act(p(FPLX:CHRN)) increases bp(GO:"circadian sleep/wake cycle, REM sleep") View Subject | View Object

Moreover, although nicotine increases wakefulness in wild-type mice, it does not affect β2−/− mice. Overall, stimulation of nAChRs promotes arousal and REM sleep. PubMed:17009926

Appears in Networks:
Annotations
MeSH
Epilepsy

p(FPLX:CHRN) increases tloc(a(CHEBI:"sodium(1+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

All the mammalian neuronal nAChR subtypes do share the general func- tional property of being permeable to small monovalent and divalent cations. The main conducting species under biological conditions are Na+, K+, and Ca2+. PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(CHEBI:"sodium(1+)"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

All the mammalian neuronal nAChR subtypes do share the general func- tional property of being permeable to small monovalent and divalent cations. The main conducting species under biological conditions are Na+, K+, and Ca2+. PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(CHEBI:"potassium(1+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

All the mammalian neuronal nAChR subtypes do share the general func- tional property of being permeable to small monovalent and divalent cations. The main conducting species under biological conditions are Na+, K+, and Ca2+. PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(CHEBI:"potassium(1+)"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

All the mammalian neuronal nAChR subtypes do share the general func- tional property of being permeable to small monovalent and divalent cations. The main conducting species under biological conditions are Na+, K+, and Ca2+. PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(CHEBI:"calcium(2+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

All the mammalian neuronal nAChR subtypes do share the general func- tional property of being permeable to small monovalent and divalent cations. The main conducting species under biological conditions are Na+, K+, and Ca2+. PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(CHEBI:"calcium(2+)"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

All the mammalian neuronal nAChR subtypes do share the general func- tional property of being permeable to small monovalent and divalent cations. The main conducting species under biological conditions are Na+, K+, and Ca2+. PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Monovalent"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations that can fit through the narrowest hydro- philic region of the open pore (Albuquerque et al., 2009; Dani, 1989; Dani & Bertrand, 2007; Dani & Eisenman, 1987). PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Monovalent"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations that can fit through the narrowest hydro- philic region of the open pore (Albuquerque et al., 2009; Dani, 1989; Dani & Bertrand, 2007; Dani & Eisenman, 1987). PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Divalent"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations that can fit through the narrowest hydro- philic region of the open pore (Albuquerque et al., 2009; Dani, 1989; Dani & Bertrand, 2007; Dani & Eisenman, 1987). PubMed:26472524

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(MESH:"Cations, Divalent"), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

Mammalian nAChRs are cation selective, being permeable to small monovalent and divalent cations that can fit through the narrowest hydro- philic region of the open pore (Albuquerque et al., 2009; Dani, 1989; Dani & Bertrand, 2007; Dani & Eisenman, 1987). PubMed:26472524

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

While nAChR activity causes depolarization, the divalent cation permeability plays an impor- tant physiological role by supplying ionic signals, including calcium (Bertrand, Galzi, Devillers-Thiery, Bertrand, & Changeux, 1993b; Dani & Bertrand, 2007; Decker & Dani, 1990; Gray, Rajan, Radcliffe, Yakehiro, & Dani, 1996; McGehee, Heath, Gelber, Devay, & Role, 1995; Vernino et al., 1992). PubMed:26472524

Appears in Networks:

act(p(FPLX:CHRN)) increases path(MESH:"Behavior, Addictive") View Subject | View Object

Although many areas of the brain participate, nicotinic receptors of the midbrain dopa- mine (DA) area are particularly important during the initiation of the addic- tion process (Dani et al., 2014; De Biasi & Dani, 2011). PubMed:26472524

Appears in Networks:
Annotations
Cell Ontology (CL)
midbrain dopaminergic neuron

act(p(FPLX:CHRN)) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Activation of the presynaptic nAChRs (commonly but not exclusively α 7 * nAChRs) enhances the release of glutamate (Dani et al., 2000; Mansvelder & McGehee, 2000, 2002). PubMed:26472524

Appears in Networks:
Annotations
MeSH
Presynaptic Terminals

p(FPLX:CHRN) hasVariant p(FPLX:CHRN, pmod(Ph)) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) decreases bp(HBP:Neurodegeneration) View Subject | View Object

Moreover, the interaction of the cholinergic and glutamatergic systems seems to be important not only for cognitive processes but also for neuroprotection, as it has been shown that nicotinic receptors agonists are neuroprotective in a mechanism that is Ca2+-dependent and that involves the glutamatergic system PubMed:26813123

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA6) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA7) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA9) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA10) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNB2) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNB3) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNB4) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) regulates bp(GO:cognition) View Subject | View Object

The neurotransmitter ACh binds to two families of receptors, nicotinic acetylcholine receptors (nAChRs) and muscarinic acetylcholine receptors (mAChRs). Both families of receptors regulate the cognitive processes mentioned above (Ghoneim and Mewaldt, 1977; Petersen, 1977; Sarter and Paolone, 2011), and are both affected in AD PubMed:25514383

Appears in Networks:

p(FPLX:CHRN) isA a(MESH:"Cysteine Loop Ligand-Gated Ion Channel Receptors") View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA2) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA3) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA4) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA5) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) regulates bp(GO:"potassium ion transport") View Subject | View Object

The five subunits that compose the receptor are assembled around a central hydrophilic pore that mediates the flow of the cations K+, Na+ and Ca++. In the human nervous system, there are eight alpha subunits (alpha2-alpha7, alpha9, alpha10) and three beta subunits (beta2-beta4) that assemble in different combinations to generate a variety of nAChR subtypes with distinct electrophysiological properties and brain localization (Albuquerque et al., 2009; Gotti et al., 2006b, 2007, 2009) PubMed:25514383

Appears in Networks:

p(FPLX:CHRN) regulates bp(GO:"sodium ion transport") View Subject | View Object

The five subunits that compose the receptor are assembled around a central hydrophilic pore that mediates the flow of the cations K+, Na+ and Ca++. In the human nervous system, there are eight alpha subunits (alpha2-alpha7, alpha9, alpha10) and three beta subunits (beta2-beta4) that assemble in different combinations to generate a variety of nAChR subtypes with distinct electrophysiological properties and brain localization (Albuquerque et al., 2009; Gotti et al., 2006b, 2007, 2009) PubMed:25514383

Appears in Networks:

p(FPLX:CHRN) regulates bp(GO:"calcium ion transport") View Subject | View Object

The five subunits that compose the receptor are assembled around a central hydrophilic pore that mediates the flow of the cations K+, Na+ and Ca++. In the human nervous system, there are eight alpha subunits (alpha2-alpha7, alpha9, alpha10) and three beta subunits (beta2-beta4) that assemble in different combinations to generate a variety of nAChR subtypes with distinct electrophysiological properties and brain localization (Albuquerque et al., 2009; Gotti et al., 2006b, 2007, 2009) PubMed:25514383

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(MESH:"Synaptic Potentials") View Subject | View Object

They demonstrated that Abeta1-42 drives a reversible inhibition of nAChR-mediated currents in hippocampal GABAergic neurons recorded from rat slices. In these experimental conditions the most effective Abeta1-42 concentration was 500 nM, but inhibition was found also at the lower concentration of 100 nM PubMed:25514383

Appears in Networks:
Annotations
Cell Ontology (CL)
GABAergic neuron
MeSH
Hippocampus

p(FPLX:CHRN) regulates path(MESH:"Cognition Disorders") View Subject | View Object

These experiments confirmed that the level of expression of APP and the consequent synthesis of Ab were comparable between mouse lines, demonstrating that the difference in cognitive deficit and neuropathology were mediated exclusively by the nicotinic recept PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:CHRN)) increases a(CHEBI:"calcium(2+)") View Subject | View Object

This kinase is sensitive to Ca++, whose levels are increased following nAChR activation (Oddo et al., 2005) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(FPLX:CHRN) association path(MESH:Arousal) View Subject | View Object

As ACh-gated cation channels, these broadly distributed receptors participate in arousal, motivation, and numerous aspects of cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996). PubMed:28445721

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Motivation) View Subject | View Object

As ACh-gated cation channels, these broadly distributed receptors participate in arousal, motivation, and numerous aspects of cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996). PubMed:28445721

Appears in Networks:

p(FPLX:CHRN) association bp(GO:cognition) View Subject | View Object

As ACh-gated cation channels, these broadly distributed receptors participate in arousal, motivation, and numerous aspects of cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996). PubMed:28445721

Appears in Networks:

p(FPLX:CHRN) increases bp(GO:cognition) View Subject | View Object

Indeed, presynaptic effects of nAChRs in regulating dopamine release in basal ganglia and prefrontal cortex likely participate in nicotine’s addictive and cognitive effects, respectively (Jasinska et al., 2014) PubMed:28445721

Appears in Networks:

p(FPLX:CHRN) association bp(GO:cognition) View Subject | View Object

Because nAChRs play important roles in cognition (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996), we focused attention on this behavi PubMed:28445721

Appears in Networks:

act(p(FPLX:CHRN)) increases act(a(MESH:"Dopaminergic Neurons")) View Subject | View Object

In substantia nigra, postsynaptic nicotinic receptors induce inward currents to excite dopaminergic neurons that project to corpus striatum (Matsubayashi et al., 2003) PubMed:28445721

Appears in Networks:
Annotations
MeSH
Substantia Nigra

p(FPLX:CHRN) increases bp(GO:"positive regulation of synaptic plasticity") View Subject | View Object

Through these postsynaptic effects and by influencing neural excitability, nAChRs can modulate or induce synaptic plasticity (Yakel, 2014) PubMed:28445721

Appears in Networks:

p(FPLX:CHRN) increases bp(GO:"dopamine secretion") View Subject | View Object

Indeed, presynaptic effects of nAChRs in regulating dopamine release in basal ganglia and prefrontal cortex likely participate in nicotine’s addictive and cognitive effects, respectively (Jasinska et al., 2014) PubMed:28445721

Appears in Networks:
Annotations
MeSH
Basal Ganglia
MeSH
Prefrontal Cortex

p(FPLX:CHRN) association path(MESH:"Tobacco Use Disorder") View Subject | View Object

Indeed, presynaptic effects of nAChRs in regulating dopamine release in basal ganglia and prefrontal cortex likely participate in nicotine’s addictive and cognitive effects, respectively (Jasinska et al., 2014) PubMed:28445721

Appears in Networks:

p(FPLX:CHRN) hasMember p(HGNC:CHRNA1) View Subject | View Object

Appears in Networks:

p(FPLX:CHRN) increases tloc(a(CHEBI:neurotransmitter), fromLoc(GO:intracellular), toLoc(GO:"extracellular region")) View Subject | View Object

Most brain HS nAChRs reside on presynaptic terminals, where they stimulate neurotransmitter release (Gotti et al., 2006; Albuquerque et al., 2009) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Presynaptic Terminals

act(p(FPLX:CHRN)) association complex(p(FPLX:CHRN), p(HGNC:LYNX1)) View Subject | View Object

As GPI-anchored proteins can bind to transmembrane receptors intracellularly, the interactions of lynx with nAChRs could potentially alter receptor trafficking, stoichiometry, and surface number (Lester et al., 2009) PubMed:21482353

Appears in Networks:

surf(p(FPLX:CHRN)) association complex(p(FPLX:CHRN), p(HGNC:LYNX1)) View Subject | View Object

As GPI-anchored proteins can bind to transmembrane receptors intracellularly, the interactions of lynx with nAChRs could potentially alter receptor trafficking, stoichiometry, and surface number (Lester et al., 2009) PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) regulates p(HGNC:LYNX1) View Subject | View Object

Abolishing receptor function through null mutations or pharmacological blockers of nAChRs abolished some of the gain-offunction phenotypes in lynx mouse models, indicating that nAChRs are necessary for the expression of lynx perturbations (Miwa et al., 2006) PubMed:21482353

Appears in Networks:

act(p(FPLX:CHRN)) negativeCorrelation act(a(MESH:Brain)) View Subject | View Object

Because excess activation of nAChRs damages neuronal health and brain function, organisms have a clear need to restrict the degree of nAChR activation PubMed:21482353

Appears in Networks:

act(p(FPLX:CHRN)) negativeCorrelation a(MESH:Neurons) View Subject | View Object

Because excess activation of nAChRs damages neuronal health and brain function, organisms have a clear need to restrict the degree of nAChR activation PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) regulates bp(GO:"GABAergic neuron differentiation") View Subject | View Object

Nicotinic receptor control over GABAergic neuronal development and mature activity may represent a point of convergence for diseases such as schizophrenia (see next section), some amblyopias (Bavelier et al., 2010), and some epilepsies (Klaassen et al., 2006), which distort the excitatory-inhibitory balance in general and implicate GABAergic signaling defects in particular PubMed:21482353

Appears in Networks:

act(p(FPLX:CHRN)) association path(MESH:"Tobacco Use Disorder") View Subject | View Object

Developmental changes in nAChR functions may play a role in nicotine addiction, as a central question in tobacco control is young adult smokers’ marked sensitivity to developing nicotine dependence (DSM-V Nicotine Workgroup, 2010; DiFranza et al., 2000; Difranza, 2010) PubMed:21482353

Appears in Networks:

act(p(FPLX:CHRN)) association path(MESH:Schizophrenia) View Subject | View Object

Recent studies provide evidence both that nicotinic signaling partially underlies these schizophrenia-related inhibitory defects and that nicotinic drugs have possible therapeutic roles PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) increases act(a(HP:"inhibitory interneuron")) View Subject | View Object

Nicotinic activation of inhibitory interneurons increases their activity and activates nitric oxide synthetase PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) increases act(p(FPLX:NOS)) View Subject | View Object

Nicotinic activation of inhibitory interneurons increases their activity and activates nitric oxide synthetase PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) association bp(GO:cognition) View Subject | View Object

Interestingly enough, a considerable body of evidence exists to suggest that the nAChRs are involved in cognitive and memory functions (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Sahakian and Coull 1994) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association bp(GO:memory) View Subject | View Object

Interestingly enough, a considerable body of evidence exists to suggest that the nAChRs are involved in cognitive and memory functions (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Sahakian and Coull 1994) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association a(MESH:"Neurotransmitter Agents") View Subject | View Object

Experimental data suggest that the nAChRs might act as neuromodulators in communicative processes in the brain (Kaiser et al 2000; Lindstro¨m 1997; Wonnacott 1997) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association path(MESH:"Alzheimer Disease") View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

A consistent, significant loss of nAChRs has been observed in cortical autopsy brain tissue from AD patients relative to age-matched healthy subjects (Nordberg and Winblad 1986) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

p(FPLX:CHRN) association path(MESH:"Parkinson Disease") View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Schizophrenia) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association path(MESH:"Tourette Syndrome") View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Anxiety) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Depression) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) association path(MESH:Epilepsy) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation path(MESH:"Cognitive Dysfunction") View Subject | View Object

The cortical nAChR deficits significantly correlate with cognitive impairment in AD patients (Nordberg, in press; Nordberg et al 1995, 1997) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Alzheimer Disease

p(FPLX:CHRN) negativeCorrelation p(HGNC:APP, var("p.Lys670Asn"), var("p.Met671Leu")) View Subject | View Object

Significant reductions in the number of nAChRs were measured in cortical regions of Swedish APP 670/ 671 mutation (273% to 287%) (Marutle et al 1999) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

p(FPLX:CHRN) negativeCorrelation a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) negativeCorrelation bp(GO:"response to oxidative stress") View Subject | View Object

Possible factors such as amyloid peptide accumulation, hyperphosphorylation of tau protein, oxidative stress, and modification of cell membrane during the development of AD may be related to decreased protein levels of nAChRs (Farooqui et al 1995; Smith et al 1996) PubMed:11230871

Appears in Networks:

act(p(FPLX:CHRN)) regulates tloc(a(CHEBI:neurotransmitter), fromLoc(GO:intracellular), toLoc(GO:"extracellular region")) View Subject | View Object

Activation of the nAChR modulates the release of several neurotransmitters (Kaiser et al 2000; Wonnacott 1997) that mediate important physiologic mechanisms including cognitive functions PubMed:11230871

Appears in Networks:

p(FPLX:CHRN) hasVariant p(FPLX:CHRN, pmod(Ph, Tyr)) View Subject | View Object

Appears in Networks:

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.