a(HBP:"alpha-7-containing nAChR")
A possible candidate is choline, which, in addition to its other development roles, activates alpha7 nAChRs at levels several fold higher than acetylcholine PubMed:21482353
A possible candidate is choline, which, in addition to its other development roles, activates alpha7 nAChRs at levels several fold higher than acetylcholine PubMed:21482353
alpha7 nAChRs are involved in the macrophage and placental cytokine response, which may be an additional role for genetic variants in these receptors in the pathogenesis of schizophrenia (Wang et al., 2003) PubMed:21482353
alpha7 nAChRs are involved in the macrophage and placental cytokine response, which may be an additional role for genetic variants in these receptors in the pathogenesis of schizophrenia (Wang et al., 2003) PubMed:21482353
Each lynx paralog has a relative binding specificity and modulatory capability on alpha4beta2 (Miwa et al., 1999; Iban˜ ez-Tallon et al., 2002; Levitin et al., 2008), alpha3 (Arredondo et al., 2006), and alpha7 (Chimienti et al., 2003; Levitin et al., 2008; Hruska et al., 2009) nAChR subtypes; some interactions actually enhance nicotinic responses (Chimienti et al., 2003; Levitin et al., 2008), or their Ca2+ components (Darvas et al., 2009) PubMed:21482353
The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871
Lee et al (2000) recently also reported a significant decrease in the alpha7 nAChR protein level of the AD hippocampus PubMed:11230871
Interestingly, a reduction in the protein level of alpha7 has also been measured in the frontal cortex of patients with schizophrenia (Guan et al 1999), whereas no decrease was measured in the alpha4 nAChR protein level (Guan et al 1999) PubMed:11230871
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
One important role for alpha7 nAChRs, in conjunction with alpha3-containing nAChRs, is the induction of the KCC2 chloride transporter in pyramidal neurons (Liu et al., 2006) PubMed:21482353
A specific role of alpha7 nAChRs was demonstrated by failure of the induction of KCC2 by treatment with alpha7 nAChR antagonists and in a7 KO mice (Zhang and Berg, 2007) PubMed:21482353
alpha7 nAChRs are involved in the macrophage and placental cytokine response, which may be an additional role for genetic variants in these receptors in the pathogenesis of schizophrenia (Wang et al., 2003) PubMed:21482353
alpha7 nAChRs are involved in the macrophage and placental cytokine response, which may be an additional role for genetic variants in these receptors in the pathogenesis of schizophrenia (Wang et al., 2003) PubMed:21482353
The levels of alpha4 and alpha7 nAChR mRNA showed a decrease with aging, whereas the levels of alpha3 mRNA were unchanged in the elderly brain relative to the fetal brain (Hellstro¨m-Lindahl et al 1998) PubMed:11230871
Lee et al (2000) recently also reported a significant decrease in the alpha7 nAChR protein level of the AD hippocampus PubMed:11230871
Interestingly, a reduction in the protein level of alpha7 has also been measured in the frontal cortex of patients with schizophrenia (Guan et al 1999), whereas no decrease was measured in the alpha4 nAChR protein level (Guan et al 1999) PubMed:11230871
Estrogen, which in epidemiologic studies has been shown to reduce the risk of AD (Henderson 1997), has in experimental studies in PC 12 cells shown neuroprotective effects against Abeta toxicity that are at least partly mediated by the alpha7 subtype nAChR (Svensson and Nordberg 1998) PubMed:11230871
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
Subsequently, renewed searches for functions of natural Bgt-binding nAChRs uncovered short-lived, nicotine-gated, toxin-sensitive, inward currents and/ or elevations of intracellular Ca2+ in chick autonomic neurons [84], in human ganglionic neuron-like clonal cells [85], or in rat CNS neurons [16,40–44,86–91]. PubMed:21787755
By virtue of their unique subcellular localizations, channel kinetics and Ca2+ permeability, a7-nAChRs appear to have novel functional roles in addition to (i.e., distinct from) the mediation of classical excitatory neurotransmission. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
For example, Bgt-sensitive a7-nAChRs have been implicated in processes such as vicinal control of neurotransmitter release [7,14], development and maintenance of neurites and synapses [18–20], long-term potentiation [95,96], seizures [97], and neuronal viability/death [21–24]. These intriguing findings underscore the need for further characterization of functional a7-nAChRs. PubMed:21787755
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