Comparison of effects of ethanol on platelet function and synaptic transmission

G. Christopher Fenn, Marina A. Lynch, Patson T. Nhamburo, Louisa Caberos, John M. Littleton

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Ethanol, at concentrations tolerated by man, is generally inhibitory to platelet function in vitro, producing significant inhibition of aggregation in response to most chemical aggregating agents. The calcium ionophore, A23187, is the agent which is most inhinited by ethanol, whereas aggregation induced by arachidonic acid is not inhibited even by concentrations of ethanol far in excess of the lethal range. This spectrum of inhibition found suggests that ethanol inhibits the platelet release reaction by a mechanism involving inhibition of Ca2+-activated phospholipase A2. These effects can be observed in superfused human platelets as well as in those suspended in buffer or in plasma. In superfused rat brain slices however, ethanol does not inhibit the A23187-induced release of radiolabelled neurotransmitter, although it can be shown to inhibit Ca2+-activated phospholipase A2 activity in rat synaptosomal preparations. It is concluded that, although there many similarities between the effects of ethanol on the platelet and the synapse there may be differences between the way in which ethanol modifies release of intracellular contents in the two situations.

Original languageEnglish
Pages (from-to)37-43
Number of pages7
JournalPharmacology Biochemistry and Behavior
Issue numberSUPPL. 1
StatePublished - 1983


  • Arachidonic acid
  • Ca ionophore A23187
  • Ethanol
  • Neurotransmitter release
  • Phospholipase
  • Platelet aggregation

ASJC Scopus subject areas

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience


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