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Entity

Name
methyllycaconitine
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 4

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

In-Edges 3

Out-Edges 16

a(MESH:methyllycaconitine) decreases act(p(HGNC:CHRNA7)) View Subject | View Object

Curiously, although most studies are in agreement that nAChRs need to be activated to mediate their protective effects, mouse cortical neurons are protected by the alpha7 antagonist methyllycaconitine (Martin et al., 2004), raising the possibility that neuroprotection by alpha7 agonists may be through desensitization rather than activation of this rapidly desensitizing receptor. This would be consistent with the alpha7- dependent activation of intracellular signaling pathways by Abeta (Bell et al., 2004), but the opposite effects on cell survival exerted by Abeta and nicotine means that other mechanisms must be sought, such as ligand-specific coupling to downstream signaling pathways. PubMed:19293145

a(MESH:methyllycaconitine) decreases act(p(HGNC:CHRNA7)) View Subject | View Object

In support of this notion, beta-estradiol protects PC12 cells from amyloid toxicity, and this is prevented when alpha7 nAChRs are blocked with methyllycaconitine (Svensson and Nordberg, 1999). PubMed:19293145

a(MESH:methyllycaconitine) increases bp(MESH:Neuroprotection) View Subject | View Object

Curiously, although most studies are in agreement that nAChRs need to be activated to mediate their protective effects, mouse cortical neurons are protected by the alpha7 antagonist methyllycaconitine (Martin et al., 2004), raising the possibility that neuroprotection by alpha7 agonists may be through desensitization rather than activation of this rapidly desensitizing receptor. This would be consistent with the alpha7- dependent activation of intracellular signaling pathways by Abeta (Bell et al., 2004), but the opposite effects on cell survival exerted by Abeta and nicotine means that other mechanisms must be sought, such as ligand-specific coupling to downstream signaling pathways. PubMed:19293145

a(MESH:methyllycaconitine) decreases path(HBP:neurotoxicity) View Subject | View Object

In support of this notion, beta-estradiol protects PC12 cells from amyloid toxicity, and this is prevented when alpha7 nAChRs are blocked with methyllycaconitine (Svensson and Nordberg, 1999). PubMed:19293145

a(MESH:methyllycaconitine) decreases act(a(MESH:"N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide")) View Subject | View Object

Notably, PHA could completely block the Ab-impaired task acquisition and reduce escape-latency to the normal level. Furthermore, the effect of PHA against the Ab-impaired task acquisition could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). It was also noted that blockade of a7 nAChR by MLA in the Gal-treated group resulted in a significant prolongation of the escape-latency on comparing with the Gal group (p<0.001) (Fig. 2). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(a(MESH:"N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide")) View Subject | View Object

MLA could completely block the PHA-induced spatial memory improvement (p<0.001). Furthermore, the effect of Gal against the Ab-impaired reference memory could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). However, a7 nAChR blockage in the Gal group has a lesser effect on reference memory in comparison of blockage of that receptor in the PHA group (p<0.05) (Fig. 4). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(a(MESH:"N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide")) View Subject | View Object

Inter-group analysis showed that the protein level decreased by pretreatment with selective a7 nAChR antagonist MLA (p<0.001). PHA and Gal prevent receptor destroying in AD animals, but this effect is completely abolished by MLA (p<0.001) (Fig. 9). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(a(CHEBI:galanthamine)) View Subject | View Object

Notably, PHA could completely block the Ab-impaired task acquisition and reduce escape-latency to the normal level. Furthermore, the effect of PHA against the Ab-impaired task acquisition could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). It was also noted that blockade of a7 nAChR by MLA in the Gal-treated group resulted in a significant prolongation of the escape-latency on comparing with the Gal group (p<0.001) (Fig. 2). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(a(CHEBI:galanthamine)) View Subject | View Object

MLA could completely block the PHA-induced spatial memory improvement (p<0.001). Furthermore, the effect of Gal against the Ab-impaired reference memory could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). However, a7 nAChR blockage in the Gal group has a lesser effect on reference memory in comparison of blockage of that receptor in the PHA group (p<0.05) (Fig. 4). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(a(CHEBI:galanthamine)) View Subject | View Object

Inter-group analysis showed that the protein level decreased by pretreatment with selective a7 nAChR antagonist MLA (p<0.001). PHA and Gal prevent receptor destroying in AD animals, but this effect is completely abolished by MLA (p<0.001) (Fig. 9). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(p(MGI:Chrna7)) View Subject | View Object

Notably, PHA could completely block the Ab-impaired task acquisition and reduce escape-latency to the normal level. Furthermore, the effect of PHA against the Ab-impaired task acquisition could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). It was also noted that blockade of a7 nAChR by MLA in the Gal-treated group resulted in a significant prolongation of the escape-latency on comparing with the Gal group (p<0.001) (Fig. 2). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(p(MGI:Chrna7)) View Subject | View Object

Effect of a7 nAChRs blockage on time spent in target quadrant in probe trials. The implications of the a7 nAChRs on PHA- or Gal-induced spatial memory enhancement were investigated by pretreatment with normal saline or MLA. A two-way ANOVA revealed significant differences of treatment [F(1,56)=4.24, p<0.05], pretreatment [F(1,56)=96.87, p<0.001] and treatment  pretreatment interaction [F(1,32)=10.69, p<0.01]. Inter-group analysis showed that this effect was blocked by the selective a7 nAChR antagonist MLA (p<0.001). PubMed:25881725

a(MESH:methyllycaconitine) decreases p(MGI:Chrna7) View Subject | View Object

Inter-group analysis showed that the protein level decreased by pretreatment with selective a7 nAChR antagonist MLA (p<0.001). PHA and Gal prevent receptor destroying in AD animals, but this effect is completely abolished by MLA (p<0.001) (Fig. 9). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown). PubMed:25881725

a(MESH:methyllycaconitine) decreases path(MESH:"Spatial Memory") View Subject | View Object

MLA could completely block the PHA-induced spatial memory improvement (p<0.001). Furthermore, the effect of Gal against the Ab-impaired reference memory could be abolished by the pre-treatment of the a7 nAChR antagonist MLA (p<0.001). However, a7 nAChR blockage in the Gal group has a lesser effect on reference memory in comparison of blockage of that receptor in the PHA group (p<0.05) (Fig. 4). PubMed:25881725

a(MESH:methyllycaconitine) causesNoChange r(MGI:Chrna7) View Subject | View Object

Also, no alterations in the expression of a7 nAChR mRNA were observed in pretreatment with normal saline or MLA in PHA- or Gal-treated groups (p>0.05). In the same way, the pattern of mRNA expression in the cortex (data not shown) was similar to the hippocampus (Fig. 7). PubMed:25881725

a(MESH:methyllycaconitine) decreases act(a(DRUGBANK:Facinicline)) View Subject | View Object

The procognitive effect of MeM-3454 on episodic memory was completely blocked by the alpha7-specific antagonist methyllycaconitine, establishing that the efficacy of MeM-3454 can be attributed to alpha7 nAChR binding. PubMed:19721446

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