Increased membrane fluidity implicated in acceleration of decay of post-tetanic potentiation by alcohols

Abstract

AFTER repetitive stimulation of a synapse, the efficacy of synaptic transmission may be potentiated for a period. In systems that lend themselves to detailed analyses, this posttetanic potentiation (PTP) has been shown to be due to an increased amount of transmitter released by the presynaptic neurone rather than to postsynaptic mechanisms¹. We have investigated the PTP of a monosynaptic, all-or-none, excitatory postsynaptic potential (e.p.s.p.) recorded in cell R15 of the abdominal ganglion of Aplysia californica with appropriate stimulation of the right visceropleural connective, and have presented evidence that the PTP of this e.p.s.p. is based on increased transmitter release². We have shown³ that while PTP is slightly prolonged by lowering the temperature of the preparation from 20 to 12 °C, the duration of the PTP is increased tenfold by further lowering of the temperature to 10 °C. This demonstration of a transition temperature suggested that the fluidity of critical lipids in the presynaptic membrane regulates the decay of PTP, such that PTP decays more slowly in conditions of decreased membrane fluidity. If this inference is correct, agents, such as alcohols⁴, that increase membrane fluidity and thus act as ‘antifreezes’, should either prevent the occurrence of the temperature transition or lower the transition temperature. These agents should also, by themselves, accelerate the rate of PTP decay and their potency should be correlated with their lipophilicity. We present here experimental evidence in support of these predictions.