Abstract
Repetitive electrical stimulation of an identified synapse in the abdominal ganglion of Aplysia californica results in post-tetanic potentiation (PTP) which decays with a single exponential time course. The rate of decay of PTP is accelerated by the initial perfusion of the abdominal ganglion with 0.8 M ethanol in seawater. Each subsequent exposure to ethanol has progressively less of an effect on the rate of decay of PTP such that, upon the fourth application (on the average), ethanol no longer accelerates the decay of PTP. If the perfusion with 0.8 M ethanol is not accompanied by stimulation of the identified synapse, tolerance does not develop. Evidence is presented which suggests that the initial exposure to ethanol accelerates the decay of PTP though fluidization of critical components of the pre-synaptic membrane. Arguments suggesting that tolerance is a compensatory change in the composition of the synaptic membrane are discussed.
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