MODULATION OF SPONTANEOUS TRANSMITTER RELEASE DURING DEPRESSION AND POSTTETANIC POTENTIATION OF APLYSIA SENSORY-MOTOR NEURON SYNAPSES ISOLATED IN CULTURE

An Aplysia motor neuron cocultured with a single presynaptic sensory n euron exhibits spontaneous miniature EPSPs or EPSCs (''minis'') that c an be used to assay the release process directly, independent of the p resynaptic action potential. Sensory-motor synapses in culture undergo homesynaptic depression with low frequency stimulation (< 1 Hz) and p osttetanic potentiation (PTP) with high-frequency stimulation (20 Hz) much as they do in intact ganglia, except that PTP does not occur in c ulture when sensory neurons are impaled. We measured spontaneous relea se during each of these two forms of homosynaptic plasticity as a way of testing whether they involve depletion or mobilization of synaptic vesicles (Gingrich and Byrne, 1985). We find that PTP is accompanied b y an increase in mini frequency that decays with a time course paralle l to the decay of evoked EPSP facilitation. In contrast, depression is not paralleled by a reduction of mini frequency, although extensive s timulation reduces mini frequency for a brief period immediately follo wing stimulation. Neither form of plasticity altered miniature EPSP or miniature EPSC amplitude, corroborating previous evidence that both a re presynaptically mediated. These findings suggest that PIP is mediat ed by a presynaptic mechanism independent of the action potential, suc h as vesicle mobilization. This presumably Ca2+-dependent mechanism do es not involve protein kinase C, since we found that the inhibitor H7 does not specifically block PTP. In contrast to PIP, depression appear s to involve changes unique to excitation-secretion coupling, such as reduced Ca2+ influx during the action potential (Klein et al., 1980).