Neuronal nicotinic acetylcholine receptors: a new target site of ethanol

@article{Narahashi1999NeuronalNA,
  title={Neuronal nicotinic acetylcholine receptors: a new target site of ethanol},
  author={Toshio Narahashi and Gary L. Aistrup and William Marszalec and Keiichi Nagata},
  journal={Neurochemistry International},
  year={1999},
  volume={35},
  pages={131-141}
}
Dual action of n-alcohols on neuronal nicotinic acetylcholine receptors.
TLDR
It is found that n-alcohols, depending on the carbon chain length, exert a dual action, potentiation and inhibition, on nnAChRs in primary cultured rat cortical neurons, suggesting that potentiating and inhibitory actions are exerted through two different binding sites.
Alcohol modulation of neuronal nicotinic acetylcholine receptors is alpha subunit dependent.
TLDR
The alpha3beta2 AChRs are insensitive to ethanol because ethanol is at the transition point from potentiation to inhibition among n-alcohols with different carbon-chain lengths, which explains the differential action of ethanol on the central nervous system.
Effects of ethanol on excitatory and inhibitory synaptic transmission in rat cortical neurons.
TLDR
It is concluded that ethanol stimulation of nAChRs modulates the activity of both glutamate and GABA receptors in rat cortical bipolar neurons.
Alcohol’s Actions on Neuronal Nicotinic Acetylcholine Receptors
  • T. Davis, C. M. de Fiebre
  • Medicine, Biology
    Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism
  • 2006
TLDR
At least one subtype of nAChR may help protect cells against alcohol-induced neurotoxicity and natural variations in the genes encoding different nA ChR subunits may be associated with individual differences in the sensitivity to some of alcohol's and nicotine's effects.
Correlation between molecular volume and effects of n-alcohols on human neuronal nicotinic acetylcholine receptors expressed in Xenopus oocytes.
TLDR
The hypothesis that molecular volume appears to be the most important determinant of both the potency as well as the direction of modulation of nAChR function by n-alcohols and related compounds is supported.
Neuronal Nicotinic Acetylcholine Receptors:Molecular Targets for Alcoholism andEthanol Reward: A Dissertation
TLDR
It is shown, for the first time, that a specific nAChR subtype, those that contain the α4 subunit (α4*), mediate voluntary ethanol consumption and reward and further supports the hypothesis that α4* nA ChRs are molecular targets for alcohol cessation therapies.
Nootropic drug modulation of neuronal nicotinic acetylcholine receptors in rat cortical neurons.
TLDR
Nefiracetam potentiating action was not affected by 24-h pretreatment of neurons with pertussis toxin, but was abolished by cholera toxin, indicating that nnAChRs are an important site of action of nefiracetAM and G(s) proteins may be its crucial target.
Acute Alcohol Action and Desensitization of Ligand-Gated Ion Channels
TLDR
Understanding interactions between ethanol and ionotropic receptor desensitization may help to explain different ethanol actions when ethanol is evaluated in vitro on cloned channel proteins, under physiological or pathological conditions or in distinct cell domains with modified ligand concentration and/or receptor conformation.
Basis of variable sensitivities of GABA(A) receptors to ethanol.
TLDR
It was concluded that the GABA(A) receptors of these four cell types were basically sensitive to n-alcohols including ethanol but the sensitivity curve was shifted to the lower side in the order of decreasing sensitivity of DRG neurons > alpha1/beta2gamma2S > cortical neurons.
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References

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Ethanol inhibition of nicotinic acetylcholine type alpha 7 receptors involves the amino-terminal domain of the receptor.
TLDR
Ethanol was found to inhibit the function of this chimeric receptor in a manner similar to that of nACh alpha 7 receptors, suggesting that the amino-terminal domain of the receptor is involved in the inhibition.
Neuronal Nicotinic Receptor Subtypes
TLDR
It is apparent that many neuronal AChRs are likely to havc functional roles that differ from the straightforward postsynaptic type of critical link in ncurotransmission exemplified by muscle ACh Rs, and the actual functional rolcs in the nervous system of many of the real and potential subtypes of neuronal A ChRs remain to be determined.
Ethanol-induced inhibition of NMDA receptor channels
Postsynaptic effects of ethanol at the frog neuromuscular junction
TLDR
The effect of ethanol on the postsynaptic membrane of the frog neuromuscular junction is investigated by measuring equilibrium dose–response curves for the interaction between the neuro-transmitter and the ACh receptors and it is found that ethanol produces significant changes in receptor function.
Ethanol modulation of nicotinic acetylcholine receptor currents in cultured cortical neurons.
Ethanol, at physiologically relevant concentrations, significantly enhanced high-affinity neuronal nicotinic acetylcholine receptor (NnAChR) currents insensitive to alpha-bungarotoxin
Mapping the location of functional nicotinic and gamma-aminobutyric acidA receptors on hippocampal neurons.
TLDR
The dendritic localization of nAChRs suggest that they are involved in modulating the synaptic efficacy at the level of the dendrites, and this morphological feature was associated with a significant decrease in the receptor density.
Blockade of nicotinic currents in hippocampal neurons defines methyllycaconitine as a potent and specific receptor antagonist.
TLDR
Low concentrations of methyllycaconitine decreased the frequency of anatoxin-induced single-channel openings, with no detectable decrease in the mean channel open time, and is commend for the characterization of the alpha-bungarotoxin-sensitive subclass of neuronal nicotinic receptors, which has hitherto eluded functional demonstration.
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