The Effect of Alcohol in the Nicotinic Acetylcholine Receptor.
- Author:
Seongho MIN
1
;
In Deok KONG
;
Seung Kyu CHA
;
Jongho SHIN
Author Information
1. Department of Psychiatry, Wonju College of Medicine, Yonsei University, Wonju, Korea. mchorock@yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Alcohol;
Nicotinic acetylcholine receptor;
Autonomic ganglion
- MeSH:
Acetylcholine;
Animals;
Bungarotoxins;
Carisoprodol;
Ethanol;
Fires;
Ganglia, Autonomic;
Ganglion Cysts;
Gramicidin;
Hexamethonium;
Humans;
Ion Channels;
Male;
Membranes;
Neurons;
Patch-Clamp Techniques;
Rats;
Receptors, Nicotinic*;
Receptors, Serotonin
- From:Korean Journal of Psychopharmacology
2006;17(1):81-90
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: It has been well known that alcohol can modulate several ligand-gated ion channel and voltage-gated ion channels. But the roles of alcohol in the autonomic neurons still remain unclear. In this study, thus we characterized the neuronal acetylcholine receptor (nnAChRs) and investigated the modulation of nnAChRs by ethanol (EtOH). METHODS: We used whole-cells which were acutely dissociated male rat major pelvic ganglion (MPG) neurons, and used gramicidin perforated patch clamp techniques. RESULTS: MPG neurons can be classified on the basis of the response of the soma membrane to depolarizing current pulses ; either tonic or phasic neurons. Sympathetic neurons expressing T-type Ca(2+) channels showed tonic firing pattern, while parasympathetic neurons lacking T-type Ca(2+) channels phasic firing to depolarizing current pulses. When hyperpolarizing currents were injected, sympathetic neurons produced post-anodal rebound spikes, while parasympathetic neurons were silent. Under current clamp mode, Acetylcholine (ACh) evoked significant membrane depolarization and produced subsequently marked membrane hyperporization. Under whole-cell mode, application of ACh-induced inward currents held at holding potentials below 0 mV and reversal potential was close to 0 mV, an equilibrium potential of nonselective cation channel. The ACh-activated current was blocked by methyllycaconitine (MLA ; 10 micrometer), hexamethonium (100 micrometer) and alpha-bungarotoxin (alpha-BuTx ; 100 nM), nAChRs antagonists. EtOH (40 mM) potentiated ACh-induced depolarization and hyperpolarization. EtOH also increased both alpha-BuTx-sensitive and -insensitive ACh-activated currents. Futhermore, EtOH potentiated 5-HT-activated current but had a little effect on GABA-activated current. CONCLUSION: These results suggest that EtOH modulates nnAChRs and 5-HT receptors in MPG neurons.
