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Entity

Name
alpha7 Nicotinic Acetylcholine Receptor
Namespace
mesh
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/8ccfed235e418e4c8aa576f9a5ef0f838e794c7f/external/mesh-names.belns

Appears in Networks 6

In-Edges 51

a(CHEBI:"amyloid-beta") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

However, alpha7 nAChR activation was observed in X. laevis oocytes when a range of Abeta concentration spanning from 1 to 100 pM was applied (Dineley et al., 2002) PubMed:25514383

a(CHEBI:"amyloid-beta polypeptide 40") decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Experiments performed on X. laevis oocytes transiently transfected with alpha7 or alpha4beta2 cDNA showed a concentration dependent effect of Abeta on receptor inhibition. In this case the peptide used was Abeta1-40 and the concentrations adopted were between 0.1 and 10 mM, with increased Abeta concentration resulting in a bigger inhibition of the receptor (Tozaki et al., 2002) PubMed:25514383

a(CHEBI:"amyloid-beta polypeptide 42") decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) 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

a(CHEBI:"amyloid-beta polypeptide 42") decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

The incubation of cultured rat hippocampal neurons with Abeta1-42 resulted in inhibition of alpha7 nAChRs, more precisely of both somato-dendritic and presynaptic populations of receptors PubMed:25514383

a(CHEBI:"amyloid-beta") decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

In this system enhancement of Akt phosphorylation and activation of ERK pathway was observed following alpha7 agonist treatment, suggesting that Abeta inhibits the neuroprotective effect of alpha7 nAChR activation (Zhi et al., 2014) PubMed:25514383

a(CHEBI:methyllycaconitine) decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Methyllycaconitine (MLA), an alpha7 nAChR antagonist, showed neuroprotective effect on mouse and rat primary cell culture (Martin et al., 2004) PubMed:25514383

a(CHEBI:nicotine) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

APPSwe mice at 14.5 months have fewer alphaBungarotoxin binding sites, while in transgenic mice treated with nicotine the number of alphaBungarotoxin binding sites was recovered and comparable to non transgenic age-matched control mice, suggesting that there was an increase in the population of alpha7 nAChRs (Hellstrom-Lindahl et al., 2004) PubMed:25514383

a(CHEBI:nicotine) increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

The explanation proposed by the authors is that alpha7 nAChR activation through nicotine binding could promote survival pathways and recover the synaptic damage caused by Abeta (Inestrosa et al., 2013) PubMed:25514383

a(CHEBI:nicotine) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Nicotine treatment improved the memory deficit, highlighted with the Morris water maze task. Surprisingly, this study showed a dose dependent increase of alpha7 nAChR, a result that is in contrast with the literature (Oddo et al., 2005) PubMed:25514383

a(HBP:"amyloid-beta 40 oligomers") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

The oligomeric form of Abeta1-40 was able to activate alpha7 nAChR expressed in SH-SY5Y cell line (Lilja et al., 2011) PubMed:25514383

a(PUBCHEM:5311278) decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

bp(GO:"calcium ion transport") positiveCorrelation a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

The subtype alpha4beta2 is characterized by lower calcium ion permeability and a slow desensitization rate compared to the homopentameric alpha7 nAChR (Quick and Lester, 2002) PubMed:25514383

bp(MESH:"Physiological Phenomena") association a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Homomeric alpha7 receptors are also abundant and are of particular interest as they show very high calcium permeability and are linked to both physiological and disease processes (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996 PubMed:28445721

p(HGNC:RIC3) increases surf(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

As previously reported using fluorescently labeled alpha-bungarotoxin (Gu et al., 2016), NACHO enabled formation of assembled surface alpha7 receptors, and RIC-3 further enhanced this (Figures 3E and 3F) PubMed:28445721

p(HGNC:TMEM35A) regulates act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Using a genomic cDNA screening strategy, we recently identified NACHO (Gu et al., 2016), a small multi-pass transmembrane protein enriched in neuronal endoplasmic reticulum (ER) that can mediate functional reconstitution of alpha7 receptors in non-neuronal cell lines PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) regulates surf(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

NACHO serves as a molecular chaperone to mediate folding, assembly, and surface expression of alpha7 receptors (Gu et al., 2016) PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) regulates a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

NACHO serves as a molecular chaperone to mediate folding, assembly, and surface expression of alpha7 receptors (Gu et al., 2016) PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

As published previously (Gu et al., 2016), ACh evoked currents from alpha7 require NACHO, and currents from alpha4beta2 were augmented ~3-fold by NACHO, which did not alter the desensitization kinetics of alpha4beta2 receptors (Figures 1A and 1B) PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) increases surf(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

As previously published (Gu et al., 2016), robust surface alpha7 and alpha4beta2 expression required co-transfection with NACHO (Figures 1C and D), and we find that alpha3beta2 is also NACHO-dependent (Figures 1C and D) PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Our previous studies demonstrated that NACHO promotes assembly of alpha7 receptors as evidenced by alpha-bungarotoxin labeling, (Gu et al., 2016) which in brain only binds with high affinity to properly folded pentameric alpha7 receptors (Couturier et al., 1990; Schoepfer et al., 1990) PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

In membranes from alpha7-transfected cells, [3H]epibatidine binding absolutely required NACHO (Figure 2A), which fits with an essential role for NACHO in alpha7 assembly PubMed:28445721

act(p(HGNC:TMEM35A), ma(chap)) increases surf(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

As previously reported using fluorescently labeled alpha-bungarotoxin (Gu et al., 2016), NACHO enabled formation of assembled surface alpha7 receptors, and RIC-3 further enhanced this (Figures 3E and 3F) PubMed:28445721

act(p(MGI:Tmem35a), ma(chap)) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Importantly, NACHO knockout mice show complete loss of alpha7 ligand binding and channel function indicating that NACHO is required for formation of alpha7 receptors (Gu et al., 2016) PubMed:28445721

path(MESH:Disease) association a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Homomeric alpha7 receptors are also abundant and are of particular interest as they show very high calcium permeability and are linked to both physiological and disease processes (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996 PubMed:28445721

a(CHEBI:choline) increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

As we will see below, the mystery of somatodendritic nAChRs can also be resolved by the sensitivity of alpha7 nAChRs to constant levels of another agonist, choline PubMed:21482353

a(CHEBI:nicotine) increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

alpha7 nAChRs also respond to nicotine concentrations roughly an order of magnitude higher than alpha42beta23, and alpha7 nAChRs have high Ca2+ permeability resembling that of NMDA receptors PubMed:21482353

a(CHEBI:nicotine) increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

While it is not yet possible to know precisely how well a7 nAChRs are activated by smoked nicotine, one can reasonably hypothesize that the patients’ higher dose of nicotine activates alpha7 nAChRs (Adler et al., 1993; Papke and Thinschmidt, 1998; Royal College of Physicians, 2007) PubMed:21482353

a(HBP:"GTS-21") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

3-(2,4 dimethoxy)-benzylidene-anabaseine, derived from an alkaloid produced by nemertine worms, is a partial agonist at alpha7 nAChRs PubMed:21482353

a(HBP:"alpha-Bungarotoxin") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

First, postmortem studies of the hippocampus and thalamus show diminished labeling of putative inhibitory neurons by alpha-bungarotoxin, an antagonist of alpha7 nAChRs (Court et al., 1999) PubMed:21482353

a(HP:"inhibitory interneuron") association a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Although alpha7 nAChRs have both presynaptic and postsynaptic expression (Frazier et al., 1998), their postsynaptic expression in humans is especially marked on inhibitory neurons of the hippocampus (Alkondon et al., 2000) PubMed:21482353

bp(GO:"calcium ion transport") association act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

alpha7 nAChRs also respond to nicotine concentrations roughly an order of magnitude higher than alpha42beta23, and alpha7 nAChRs have high Ca2+ permeability resembling that of NMDA receptors PubMed:21482353

g(HGNC:NRG1) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Yet some of the other genes identified, such as NRG1, are involved in the assembly of alpha7 nAChRs, further supporting a potential link between alpha7 nAChRs and schizophrenia (Mathew et al., 2007) PubMed:21482353

path(MESH:Schizophrenia) association a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

Yet some of the other genes identified, such as NRG1, are involved in the assembly of alpha7 nAChRs, further supporting a potential link between alpha7 nAChRs and schizophrenia (Mathew et al., 2007) PubMed:21482353

a(HBP:"B-973") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Peak current was increased 2-fold and 6-fold relative to 3 mM acetylcholine in 300 nM and 1 μM B-973, respectively (Fig. 1C) PubMed:28132910

a(HBP:"B-973") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

The amplitude of currents were dose dependent, reaching levels at 30 μM B-973 larger than control currents in response to 3 mM acetylcholine (Fig. 7A) PubMed:28132910

a(HBP:"B-973") increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

The currents induced by B-973 alone arise from the α7 receptor since methyllycaconitine blocks them nearly completely (Fig. 7C and Fig. S6) PubMed:28132910

a(PUBCHEM:5288811) decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

The currents induced by B-973 alone arise from the α7 receptor since methyllycaconitine blocks them nearly completely (Fig. 7C and Fig. S6) PubMed:28132910

a(MESH:Microglia) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

We next tested the impact of anatabine on STAT3 and p65 NFkB phosphorylation induced by a 24 h treatment with LPS on human microglial cells, a cell type known to express alpha7-nicotinic acetylcholine receptor subtype (Suzuki et al., 2006) PubMed:23178521

a(CHEBI:varenicline) increases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Varenicline (Chantix®; Fig. 4) is prescribed as an adjunct medication in smoking cessation therapy and is thought to exert its effects as a partial agonist at α4β2 nAChRs and as a full agonist at α7 nAChRs [211, 212]. PubMed:28391535

a(MESH:"Dihydro-beta-Erythroidine") decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

For example, DHβE (at nM concentrations) blocks α4β2 and α3β2 nAChRs but is much less potent at α3β4 and α7 nAChRs expressed in Xenopus oocytes (e.g., [134–137]). PubMed:28391535

a(PUBCHEM:5288811) decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

This conclusion is based on the fact that the stimulus effects of nicotine are convincingly blocked by (a) mecamylamine, a voltage dependent noncompetitive channel blocker at nicotinic receptors (Fig. 3; Table 4) and (b) dihydro-β-erythrodine (DHβE), a nicotinic receptor antagonist that shows high affinity for the nAChR α4β2 subunit (Fig. 3; Table 5) but not by methyllycaconitine (MLA), a α7 nicotinic receptor antagonist (Table 5). PubMed:28391535

a(PUBCHEM:5288811) decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Its biochemical pharmacology indicates that it is a relatively potent competitive receptor antagonist that is selective for α7 nAChRs (e.g., [139–141]). PubMed:28391535

Out-Edges 36

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"calcium ion transport") View Subject | View Object

The alpha7 homomeric receptor demonstrates a wide-spread localization in the brain and is characterized by a high calcium ion permeability and a fast desensitization rate (Dani and Bertrand, 2007; Quick and Lester, 2002) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") positiveCorrelation bp(GO:"calcium ion transport") View Subject | View Object

The subtype alpha4beta2 is characterized by lower calcium ion permeability and a slow desensitization rate compared to the homopentameric alpha7 nAChR (Quick and Lester, 2002) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") regulates tloc(a(CHEBI:neurotransmitter), fromLoc(MESH:"Intracellular Space"), toLoc(MESH:"Extracellular Space")) View Subject | View Object

alpha7 nAChR on presynaptic terminals mediate release of others neurotransmitters (Wonnacott et al., 2006), while a postsynaptic or somatic localization elicits important changes in intracellular Ca++ concentration, that can activate second messenger pathways mediating cellular processes such as neuronal survival and gene expression (Berg and Conroy, 2002; Messi et al., 1997; Morley and Happe, 2000) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") regulates bp(GO:"second-messenger-mediated signaling") View Subject | View Object

alpha7 nAChR on presynaptic terminals mediate release of others neurotransmitters (Wonnacott et al., 2006), while a postsynaptic or somatic localization elicits important changes in intracellular Ca++ concentration, that can activate second messenger pathways mediating cellular processes such as neuronal survival and gene expression (Berg and Conroy, 2002; Messi et al., 1997; Morley and Happe, 2000) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") regulates bp(GO:"neuron cellular homeostasis") View Subject | View Object

alpha7 nAChR on presynaptic terminals mediate release of others neurotransmitters (Wonnacott et al., 2006), while a postsynaptic or somatic localization elicits important changes in intracellular Ca++ concentration, that can activate second messenger pathways mediating cellular processes such as neuronal survival and gene expression (Berg and Conroy, 2002; Messi et al., 1997; Morley and Happe, 2000) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") regulates bp(GO:"gene expression") View Subject | View Object

alpha7 nAChR on presynaptic terminals mediate release of others neurotransmitters (Wonnacott et al., 2006), while a postsynaptic or somatic localization elicits important changes in intracellular Ca++ concentration, that can activate second messenger pathways mediating cellular processes such as neuronal survival and gene expression (Berg and Conroy, 2002; Messi et al., 1997; Morley and Happe, 2000) PubMed:25514383

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) increases a(GO:"glutamatergic synapse") View Subject | View Object

Moreover, it was demonstrated that the activation of alpha7 nAChRs is important during development for the maturation of glutamatergic synapses (Lozada et al., 2012) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases tloc(a(CHEBI:"calcium(2+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) View Subject | View Object

In a different study, rat hippocampus and cortex were investigated and the activation of both alpha7 and non-alpha7 receptors was obtained with an enhancement of Ca++ influx into the neuron following the application of picomolar (pM) concentrations of Abeta1-42 PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"positive regulation of synaptic plasticity") View Subject | View Object

This enhancement of synaptic plasticity and the activation of intracellular pathways are mediated by the activation of alpha7 nAChRs (Dineley et al., 2001; Parri et al., 2011; Plant et al., 2003; Puzzo et al., 2008) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"intracellular signal transduction") View Subject | View Object

This enhancement of synaptic plasticity and the activation of intracellular pathways are mediated by the activation of alpha7 nAChRs (Dineley et al., 2001; Parri et al., 2011; Plant et al., 2003; Puzzo et al., 2008) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases p(FPLX:AKT, pmod(Ph)) View Subject | View Object

In this system enhancement of Akt phosphorylation and activation of ERK pathway was observed following alpha7 agonist treatment, suggesting that Abeta inhibits the neuroprotective effect of alpha7 nAChR activation (Zhi et al., 2014) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"ERK1 and ERK2 cascade") View Subject | View Object

In this system enhancement of Akt phosphorylation and activation of ERK pathway was observed following alpha7 agonist treatment, suggesting that Abeta inhibits the neuroprotective effect of alpha7 nAChR activation (Zhi et al., 2014) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") decreases bp(HP:Neurodegeneration) View Subject | View Object

In this system enhancement of Akt phosphorylation and activation of ERK pathway was observed following alpha7 agonist treatment, suggesting that Abeta inhibits the neuroprotective effect of alpha7 nAChR activation (Zhi et al., 2014) PubMed:25514383

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) increases bp(HP:Neurodegeneration) View Subject | View Object

Methyllycaconitine (MLA), an alpha7 nAChR antagonist, showed neuroprotective effect on mouse and rat primary cell culture (Martin et al., 2004) PubMed:25514383

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) increases bp(MESH:"Cell Survival") View Subject | View Object

The explanation proposed by the authors is that alpha7 nAChR activation through nicotine binding could promote survival pathways and recover the synaptic damage caused by Abeta (Inestrosa et al., 2013) PubMed:25514383

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) increases a(GO:synapse) View Subject | View Object

The explanation proposed by the authors is that alpha7 nAChR activation through nicotine binding could promote survival pathways and recover the synaptic damage caused by Abeta (Inestrosa et al., 2013) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases act(a(CHEBI:simvastatin)) View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:memory) View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") decreases bp(GO:"apoptotic process") View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"calcium ion transport") View Subject | View Object

Homomeric alpha7 receptors are also abundant and are of particular interest as they show very high calcium permeability and are linked to both physiological and disease processes (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996 PubMed:28445721

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") association bp(MESH:"Physiological Phenomena") View Subject | View Object

Homomeric alpha7 receptors are also abundant and are of particular interest as they show very high calcium permeability and are linked to both physiological and disease processes (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996 PubMed:28445721

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") association path(MESH:Disease) View Subject | View Object

Homomeric alpha7 receptors are also abundant and are of particular interest as they show very high calcium permeability and are linked to both physiological and disease processes (Gotti and Clementi, 2004; Hogg et al., 2003; Le Nove` re et al., 2002; Lindstrom, 1997; Picciotto, 2003; Role and Berg, 1996 PubMed:28445721

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) association bp(GO:"calcium ion transport") View Subject | View Object

alpha7 nAChRs also respond to nicotine concentrations roughly an order of magnitude higher than alpha42beta23, and alpha7 nAChRs have high Ca2+ permeability resembling that of NMDA receptors PubMed:21482353

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) increases act(p(MGI:Lynx1)) View Subject | View Object

Evidence thus far indicates that the lynx family is regulated in response to relatively strong perturbations: downregulation in NKCC1 knockout mice (Pfeffer et al., 2009), in adenylyl cyclase mutant mice (Wieczorek et al., 2010), and by alpha7 nAChR blockade (Hruska et al., 2009), whereas it is upregulated at the close of the critical period in the visual cortex, and by nicotine in the lung (Sekhon et al., 2005) PubMed:21482353

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") regulates bp(GO:"sensory processing") View Subject | View Object

alpha7 nAChRs on inhibitory interneurons throughout the hippocampus and presynaptic alpha7 nAChRs on mossy fiber terminals in the dentate gyrus participate in the control of sensory response in the hippocampus (Gray et al., 1996; Alkondon et al., 1999 PubMed:21482353

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:"sensory processing") View Subject | View Object

Three lines of evidence support the possibility that the failure of sensory inhibition in schizophrenia results from decreased expression of alpha7 nAChRs PubMed:21482353

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") association a(HP:"inhibitory interneuron") View Subject | View Object

Although alpha7 nAChRs have both presynaptic and postsynaptic expression (Frazier et al., 1998), their postsynaptic expression in humans is especially marked on inhibitory neurons of the hippocampus (Alkondon et al., 2000) PubMed:21482353

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases a(HP:"inhibitory interneuron") View Subject | View Object

First, postmortem studies of the hippocampus and thalamus show diminished labeling of putative inhibitory neurons by alpha-bungarotoxin, an antagonist of alpha7 nAChRs (Court et al., 1999) PubMed:21482353

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") association path(MESH:Schizophrenia) View Subject | View Object

Yet some of the other genes identified, such as NRG1, are involved in the assembly of alpha7 nAChRs, further supporting a potential link between alpha7 nAChRs and schizophrenia (Mathew et al., 2007) PubMed:21482353

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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.