Effects of Ethanol on Electrolyte Metabolism and Neurotransmitter Release in the CNS

  • Y. Israel
  • F. J. Carmichael
  • J. A. Macdonald
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 59)


It has been reported that ethanol inhibits the movements of Na and K in the nerve action potential (Armstrong and Binstock, 1964; Moore et al., 1964) and also inhibits the active transport of these two ions (Israel et al, 1971). However, there is disagreement as to which of these processes is inhibited more effectively by pharmacologically relevant concentrations of ethanol (Israel et al, 1971; Wallgren, 1971; Israel et al, 1973). The active accumulation of several neurotransmitters including norepinephrine, glutamate and serotonin, has also been shown to be inhibited by ethanol, although concentrations in the lethal range are required for these effects (Israel et al, 1973; Roach et al, 1973). There is relatively little information as to the effects of ethanol on neurotransmitter release, and there is controversy in this aspect. For example, the passive (spontaneous) release of acetylcholine (ACh) has been reported to be inhibited by ethanol in brain slices (Kalant et al, 1967; Kalant and Grose, 1967) but to be increased by this drug in the neuromuscular junction (Gage, 1965; Okada, 1967; Inoue and Frank, 1967). On the other hand, it has been reported that in vivo ethanol inhibits the release of ACh from brain cortex and midbrain regions, (Phillis and Jhamandas, 1971; Erickson and Graham, 1973).


Electrical Stimulation Brain Slice Neurotransmitter Release Brain Cortical Slice Steady State Base 
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Copyright information

© Springer Science+Business Media New York 1975

Authors and Affiliations

  • Y. Israel
    • 1
  • F. J. Carmichael
    • 1
  • J. A. Macdonald
    • 1
  1. 1.Dept. PharmacologyUniversity of Toronto and Addiction Research FoundationTorontoCanada

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