Non-monotonic decay of excitatory synaptic transmission in the frog optic tectum following repetitive stimulation of the optic nerve in vitro.

The monosynaptic field excitatory postsynaptic potentials (EPSPs) evoked in the optic tectum of the frog (Rana remporaria) in vitro by different patterns of stimulation of the contralateral optic nerve were studied using extracellular recording. Pulse trains at frequencies of less than or equal to 0.033 Hz elicited field potentials of stable amplitude, whereas in the range 0.33-1.0 Hz EPSPs showed a depression in the first few responses subsequent to the first one, followed by a partial recovery and a final decline to a steady level. When the interpulse interval was less than 200 ms, paired-pulse monosynaptic facilitation was found. Decrease in the external Ca2+ concentration, or in the stimulation intensity or application of picrotoxin reversibly produced a monotonically decreasing EPSP amplitude, suggesting that a local neuronal circuit was controlling the development of synaptic fatigue. A simple model based on the combined effects of depletion of excitatory transmitter stores plus activation of a local inhibitory circuit was found to provide a simulation which closely resembled the experimentally observed pattern of synaptic fatigue. The present study suggests that an inhibitory synaptic process contributed to the non-monotonic decay of excitatory transmission in the frog optic tectum, following repetitive stimulation of the optic nerve.