Alcohol and General Anesthetic Modulation of Gabaa and Neuronal Nicotinic Acetylcholine Receptors
A number of studies have been performed during the past ten years or so in an attempt to elucidate the cellular and molecular mechanisms of action of alcohols and general anesthetics. One of the many questions asked is which receptor(s) and channel(s) is (are) the important target sites of alcohols. The history of the study of alcohol-channel interactions goes back to 1964 when Armstrong and Binstock (1964) and Moore et al. (1964) found that ethanol and higher alcohols suppressed both sodium and potassium currents in squid giant axons. The potency of ethanol was very low, and at 650 mM and 1300 mM it suppressed the sodium current only by 18% and 41%, respectively (Moore et al., 1964). The general anesthetic halothane is also known to inhibit sodium and potassium currents in squid giant axons only at concentrations much higher than those that cause clinical anesthesia (Franks and Lieb, 1994).
KeywordsSquid Giant Axon Neuronal Nicotinic Acetylcholine Receptor Subunit Combination PCI2 Cell Receptor Single Channel
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