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a(MESH:Nicotine)

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Entity

Name
Nicotine
Namespace
mesh
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/mesh-names.belns

Appears in Networks 1

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

In-Edges 12

a(HBP:cytisine) decreases act(a(MESH:Nicotine)) View Subject | View Object

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

Appears in Networks:

a(MESH:"Dihydro-beta-Erythroidine") decreases act(a(MESH:Nicotine)) View Subject | View Object

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

Appears in Networks:

a(MESH:"Dopaminergic Neurons") regulates a(MESH:Nicotine) View Subject | View Object

Dopamine (DA) neurons, which project to the NAc receive both excitatory glutamater- gic and cholinergic afferents that mediate nicotine reward, and inhibitory GABAergic afferents, that mediate aversion [77]. The release of these neurotransmitters is modulated by the nAChRs expressed in cholinergic, glutamatergic and GABAergic terminals PubMed:28901280

Appears in Networks:

a(MESH:Carbachol) decreases act(a(MESH:Nicotine)) View Subject | View Object

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

Appears in Networks:

a(MESH:Mecamylamine) decreases act(a(MESH:Nicotine)) View Subject | View Object

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

Appears in Networks:

a(MESH:Varenicline) decreases act(a(MESH:Nicotine)) View Subject | View Object

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

Appears in Networks:

complex(a(MESH:Nicotine), p(MESH:"Receptors, Nicotinic")) hasComponent a(MESH:Nicotine) View Subject | View Object

Appears in Networks:

g(DNSNP:rs16969968) association act(a(MESH:Nicotine)) View Subject | View Object

The coding SNP α5 D398N is closely associated with nicotine consumption PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

p(MGI:Chrna2) increases a(MESH:Nicotine) View Subject | View Object

Finally, a study has shown that α2 Ko mice have enhanced nicotine self-administration behaviour [88]. These findings suggest that α5* nAChRs in the MHb, and α2* nAChRs in the IPN may underlie aversive responses to nicotine. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

p(MGI:Chrna5) regulates act(a(MESH:Nicotine)) View Subject | View Object

α5 subunit Ko mice or mice with selective knock down of the α5 subunits in the Hb develop increased nicotine intake in a self-administration paradigm that is blocked by the selective re-expression of the α5 subunit within the MHb; thus indicating that the α5-containing nAChRs located in this brain area also play an important role in regulating the negative effects of nicotine. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

p(MGI:Chrna5) increases a(MESH:Nicotine) View Subject | View Object

Finally, a study has shown that α2 Ko mice have enhanced nicotine self-administration behaviour [88]. These findings suggest that α5* nAChRs in the MHb, and α2* nAChRs in the IPN may underlie aversive responses to nicotine. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

p(MGI:Chrnb4) decreases act(a(MESH:Nicotine)) View Subject | View Object

On the contrary the overexpression of β4* nAChRs in mice decreases nico- tine reinforcing properties and consumption PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

Out-Edges 22

a(MESH:Nicotine) decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

α4β2* subtypes, in which the presence of different accessory subunits changes their pharmacological and biophysical properties, and their sensitivity to allosteric modulators and up-regulation by nicotine PubMed:28901280

Appears in Networks:

a(MESH:Nicotine) increases complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

By activating the α4β2 receptors on inhibitory GABAergic inputs to the VTA or GABAergic interneurons, smoked concentrations of nicotine transiently increase the release of GABA and subse- quently depress it for about one hour PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) decreases a(MESH:Neurons) View Subject | View Object

nAChRs are particularly important in two critical periods of brain life: early pre- and post-natal circuit formation, and age-related cell degeneration. They are involved in neuronal survival, as it has been shown that nicotinic agonists are neu- roprotective in in vivo and in vitro models PubMed:28901280

Appears in Networks:

a(MESH:Nicotine) decreases p(MESH:"Receptors, Nicotinic") View Subject | View Object

Chronic nicotine exposure induces neural adaptations that change cell physi- ology and behaviour mainly as a result of activation and/or desensitisation of nAChRs. Studies of the brains of animals and smokers chronically exposed to nicotine have shown an increase in the number of nAChRs (up-regulation). PubMed:28901280

Appears in Networks:

a(MESH:Nicotine) increases bp(GO:"nodal receptor complex assembly") View Subject | View Object

There is evidence indicating that key steps in nicotine-induced up-regulation are receptor assem- bly [72, 73], decreased proteasomal degradation [74], traf- ficking [75] and cell surface expression PubMed:28901280

Appears in Networks:

a(MESH:Nicotine) increases act(p(MESH:"Proteasome Endopeptidase Complex")) View Subject | View Object

There is evidence indicating that key steps in nicotine-induced up-regulation are receptor assem- bly [72, 73], decreased proteasomal degradation [74], traf- ficking [75] and cell surface expression PubMed:28901280

Appears in Networks:

a(MESH:Nicotine) increases a(MESH:Glutamates) View Subject | View Object

By acting on the α7 receptors in glutamate terminals, acutely administrated nicotine stimu- lates the release of glutamate, which facilitates the burst fir- ing of VTA DA neurons and eventually leads to LTP,and increases the firing rate of the GABAergic neurons of the rostromedial tegmental nucleus PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases a(MESH:Glutamates) View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases p(MESH:"Receptors, GABA") View Subject | View Object

By activating the α4β2 receptors on inhibitory GABAergic inputs to the VTA or GABAergic interneurons, smoked concentrations of nicotine transiently increase the release of GABA and subse- quently depress it for about one hour PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) decreases p(MESH:"Receptors, GABA") View Subject | View Object

By activating the α4β2 receptors on inhibitory GABAergic inputs to the VTA or GABAergic interneurons, smoked concentrations of nicotine transiently increase the release of GABA and subse- quently depress it for about one hour PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases bp(GO:"action potential initiation") View Subject | View Object

nicotine modulates the shift towards burst firing and increases DA release in the NAc PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases a(MESH:Dopamine) View Subject | View Object

nicotine modulates the shift towards burst firing and increases DA release in the NAc PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases a(MESH:Dopamine) View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases act(p(HGNC:CHRNA7)) View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

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

These alterations are very similar to those observed in cul- tured human airway cells or in ex vivo human lung explants treated with the selective α7 antagonist αBgtx, or epithelial cell cultures chronically exposed to nicotine in which nico- tine-induced desensitisation of α7 receptors mimics the ab- sence of α7 nAChR PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases p(MESH:"Receptors, N-Methyl-D-Aspartate") View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases bp(MESH:"Long-Term Potentiation") View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

act(a(MESH:Nicotine)) association g(DNSNP:rs16969968) View Subject | View Object

The coding SNP α5 D398N is closely associated with nicotine consumption PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases path(MESH:Neoplasms) View Subject | View Object

When lung cancer arises from the airway epithelium, cell growth is stimulated by ACh or nicotine, and this growth loop may provide endogenous mitogenic signalling without any further activation PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) causesNoChange act(complex(p(HGNC:CHRNA10), p(HGNC:CHRNA9))) View Subject | View Object

α9 and α9-α10 nAChRs have a number of interesting characteristics: they are acti- vated by ACh but not by the classical agonist nicotine. Cho- line is also a potent selective agonist of the α9 subtype PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) causesNoChange act(p(HGNC:CHRNA9)) View Subject | View Object

α9 and α9-α10 nAChRs have a number of interesting characteristics: they are acti- vated by ACh but not by the classical agonist nicotine. Cho- line is also a potent selective agonist of the α9 subtype PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

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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.