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p(MGI:Chrna7)

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Entity

Name
Chrna7
Namespace
mgi
Namespace Version
20181021
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/f2f993e599694ab5ce989cc39d789a499f75db99/external/mgi-names.belns

Appears in Networks 7

albuquerque2009 v1.0.0

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

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. 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

B-973, a novel piperazine positive allosteric modulator of the α7 nicotinic acetylcholine receptor v1.0.0

Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice v1.0.0

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

In-Edges 18

complex(a(CHEBI:"amyloid-beta"), p(MGI:Chrna7)) hasComponent p(MGI:Chrna7) View Subject | View Object

Appears in Networks:

a(CHEBI:"kynurenic acid") decreases act(p(MGI:Chrna7, loc(MESH:Interneurons))) View Subject | View Object

Mice with a null mutation in the gene that encodes KAT II became a unique tool to resolve this issue (31, 410, 516). Low levels of KYNA in these mutant mice lead to alpha7 nAChR disinhibition in hippocampal CA1 SR interneurons, thereby increasing the activity of GABAergic interneurons impinging onto CA1 pyramidal neurons (31) PubMed:19126755

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
Text Location
Review

path(MESH:Aging) negativeCorrelation p(MGI:Chrna7) View Subject | View Object

Mouse strains, like humans, also exhibit a striking age-related decline in nAChR expression. For instance, in the hippocampus of aged CBA and B6 mice, expression of alpha4 and alpha7 nAChR subunits decreases with age (166). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Hippocampus
Text Location
Review

path(MESH:"Alzheimer Disease") causesNoChange p(MGI:Chrna7) View Subject | View Object

Tg2576 mice expressing human Abeta show reduced [3H]cytisine binding (a label of nAChRs) in the cortex at 17 months after birth (Apelt et al., 2002). In contrast, however, levels of alpha7 or alpha4 subunits were unchanged in double-mutant Swedish APP/PS-1 mice as determined by radiolabeled cytosine (alpha4beta2) or alpha-bungarotoxin (alpha7) binding (Marutle et al., 2002). PubMed:19293145

Appears in Networks:

complex(a(CHEBI:"amyloid-beta polypeptide 40"), p(MGI:Chrna7)) hasComponent p(MGI:Chrna7) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta polypeptide 42"), p(MGI:Chrna7)) hasComponent p(MGI:Chrna7) View Subject | View Object

Appears in Networks:

bp(GO:aging) association p(MGI:Chrna7) View Subject | View Object

However, we identify a possible role of the alpha7 subunit in the normal aging process that should be further investigated PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

composite(p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")), p(MGI:Chrna7)) hasComponent p(MGI:Chrna7) View Subject | View Object

Appears in Networks:

complex(a(PUBCHEM:16068384), p(MGI:Chrna7)) hasComponent p(MGI:Chrna7) View Subject | View Object

Appears in Networks:

a(CHEBI:galanthamine) increases p(MGI:Chrna7) View Subject | View Object

The analysis also showed significant effects of PHA and Gal on the protein levels on comparing with normal saline in AD mice (p<0.001). Moreover, Gal could not completely protect the a7 nAChR protein level in AD animals. This group has a lesser a7 nAChR protein level in comparison with the control group (p<0.001) (Fig. 8). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown) PubMed:25881725

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:galanthamine) increases 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

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(MESH:"N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide") increases p(MGI:Chrna7) View Subject | View Object

The analysis also showed significant effects of PHA and Gal on the protein levels on comparing with normal saline in AD mice (p<0.001). Moreover, Gal could not completely protect the a7 nAChR protein level in AD animals. This group has a lesser a7 nAChR protein level in comparison with the control group (p<0.001) (Fig. 8). The groups showed results in the cortex similar to those observed in the hippocampus (data not shown) PubMed:25881725

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(MESH:"N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide") increases 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

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") negativeCorrelation p(MGI:Chrna7) View Subject | View Object

Post hoc analysis revealed that, levels of the a7 nAChR protein in normal saline-treated AD mice were significantly lower than its level in the control animals (p<0.001). PubMed:25881725

Appears in Networks:

act(a(MESH:Epithelium)) association p(MGI:Chrna7) View Subject | View Object

α7 nAChRs are essential for the plasticity of the airway epithelium as α7 Ko mice show altered basal cell layer formation, hyperplasia, and uncontrolled growth PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

Out-Edges 21

act(p(MGI:Chrna7, loc(MESH:Interneurons))) increases act(a(MESH:"GABAergic Neurons")) View Subject | View Object

Mice with a null mutation in the gene that encodes KAT II became a unique tool to resolve this issue (31, 410, 516). Low levels of KYNA in these mutant mice lead to alpha7 nAChR disinhibition in hippocampal CA1 SR interneurons, thereby increasing the activity of GABAergic interneurons impinging onto CA1 pyramidal neurons (31) PubMed:19126755

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
Text Location
Review

p(MGI:Chrna7) negativeCorrelation path(MESH:Aging) View Subject | View Object

Mouse strains, like humans, also exhibit a striking age-related decline in nAChR expression. For instance, in the hippocampus of aged CBA and B6 mice, expression of alpha4 and alpha7 nAChR subunits decreases with age (166). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Hippocampus
Text Location
Review

p(MGI:Chrna7) increases bp(MESH:"Neuronal Outgrowth") View Subject | View Object

For example, a recent study has shown that alpha7-specific ligands rescue the Abeta-induced decrease in neurite outgrowth of cultured mouse neurons (Hu et al., 2007). PubMed:19293145

Appears in Networks:

p(MGI:Chrna7) decreases path(MESH:"Spatial Memory") View Subject | View Object

This AD model displays spatial memory deficit at 13-16 months of age, while APP-alpha7KO mice did not exhibit any memory deficit, suggesting that the absence of the alpha7 subunit of the nicotinic receptor protects against the behavioural deficit caused by expression of the mutated forms of APP in this AD model PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) decreases p(MGI:Syp) View Subject | View Object

In the APP-alpha7KO line the lack of alpha7 was sufficient to preserve synaptic terminals and dendrites, rescuing levels of synaptophysin and MAP2 to reach that of aged-matched WT controls PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) decreases p(MGI:Map2) View Subject | View Object

In the APP-alpha7KO line the lack of alpha7 was sufficient to preserve synaptic terminals and dendrites, rescuing levels of synaptophysin and MAP2 to reach that of aged-matched WT controls PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) increases p(MGI:Map2) View Subject | View Object

Signs of neuropathology were found in APP-alpha7KO illustrated by loss of MAP2 immunoreactivity in the hippocampus PubMed:25514383

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(MGI:Chrna7) increases a(CHEBI:"amyloid-beta") View Subject | View Object

The authors postulated that the absence of alpha7 could prevent Abeta intracellular accumulation ameliorating the cognitive neuropathology and its phenotypic association (Dziewczapolski et al., 2009) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

In the hippocampus, it was shown that APP-alpha7KO mice had high levels of Abeta, although significantly less than APP mice, an effect which is not due to modification of the APP expression level,equivalent in the two lines PubMed:25514383

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(MGI:Chrna7) increases bp(GO:cognition) View Subject | View Object

The authors postulated that the absence of alpha7 could prevent Abeta intracellular accumulation ameliorating the cognitive neuropathology and its phenotypic association (Dziewczapolski et al., 2009) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) decreases path(MESH:"Cognition Disorders") View Subject | View Object

The contextual fear conditioning and the novel object recognition tasks both showed that the cognitive deficits worsen when alpha7 is absent PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) increases path(MESH:"Plaque, Amyloid") View Subject | View Object

As a consequence of the lower Abeta concentration, the plaque load was clearly reduced in APP-alpha7KO mice PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MGI:Chrna7) decreases path(MESH:"Memory Disorders") View Subject | View Object

Noninjected mice spent the same amount of time exploring novel and familiar compartments during the test session (p = 0.6; Fig. 5C), confirming the presence of a constitutive recognition memory deficit in age-matched alpha7 KO mice PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

p(MGI:Chrna7) decreases path(MESH:"Memory Disorders") View Subject | View Object

Because the alpha7 KO had a memory deficit independent of hAPP-SLA expression, we could not draw any conclusion on the role of alpha7 in the memory deficit observed PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

p(MGI:Chrna7) decreases path(MESH:"Cognitive Dysfunction") View Subject | View Object

In the NOR task (15 months p.i.) as well, both GFP-alpha7 and APP-alpha7 displayed a cognitive impairment (Fig. 5DeE) PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

p(MGI:Chrna7) association bp(GO:aging) View Subject | View Object

However, we identify a possible role of the alpha7 subunit in the normal aging process that should be further investigated PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

p(MGI:Chrna7) increases a(HBP:HBP00022) View Subject | View Object

Immunofluorescence performed with VHH 31-1 on brain slices of APP-alpha7 mice also showed intracellular Abeta oligomers in the polymorphic layer (Fig. 8, arrows), whereas GFP-alpha7 mice did not show any Abeta oligomers PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

act(p(MGI:Chrna7)) increases bp(GO:learning) 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

Appears in Networks:

act(p(MGI:Chrna7)) increases path(MESH:"Spatial Memory") 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

Appears in Networks:

p(MGI:Chrna7) negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Post hoc analysis revealed that, levels of the a7 nAChR protein in normal saline-treated AD mice were significantly lower than its level in the control animals (p<0.001). PubMed:25881725

Appears in Networks:

p(MGI:Chrna7) association act(a(MESH:Epithelium)) View Subject | View Object

α7 nAChRs are essential for the plasticity of the airway epithelium as α7 Ko mice show altered basal cell layer formation, hyperplasia, and uncontrolled growth PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

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