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Title: Depression of glutamate-mediated synaptic transmission by benzyl alcohol. Author: Colton CA, Colton JS. Journal: Can J Physiol Pharmacol; 1977 Aug; 55(4):917-22. PubMed ID: 198078. Abstract: The data obtained from this study suggest that the nonionizable anesthetic benzyl alcohol has two prominent actions on GABA- and glutamate-mediated synaptic transmission at the lobster neuromuscular junction. They are as follows: (1) depression of the excitatory end-plate potential and the postsynaptic membrane response to applied glutamate, and (2) a hyperpolarization of the postsynaptic resting membrane potential associated with a decrease in effective membrane resistance. No change in amplitude of the inhibitory end-plate potential or inhibitory reversal potential was seen. Excitatory miniature end-plate potential frequency was also unaffected. The depression of excitatory synaptic transmission appears to be due to a decreased responsiveness of the postsynaptic receptor-ionophore complex.[Abstract] [Full Text] [Related] [New Search]