PT - JOURNAL ARTICLE AU - LS Eliot AU - ER Kandel AU - RD Hawkins TI - Modulation of spontaneous transmitter release during depression and posttetanic potentiation of Aplysia sensory-motor neuron synapses isolated in culture AID - 10.1523/JNEUROSCI.14-05-03280.1994 DP - 1994 May 01 TA - The Journal of Neuroscience PG - 3280--3292 VI - 14 IP - 5 4099 - http://www.jneurosci.org/content/14/5/3280.short 4100 - http://www.jneurosci.org/content/14/5/3280.full SO - J. Neurosci.1994 May 01; 14 AB - An Aplysia motor neuron cocultured with a single presynaptic sensory neuron exhibits spontaneous miniature EPSPs or EPSCs (“minis”) that can be used to assay the release process directly, independent of the presynaptic action potential. Sensory-motor synapses in culture undergo homosynaptic depression with low frequency stimulation (< 1 Hz) and posttetanic potentiation (PTP) with high-frequency stimulation (20 Hz) much as they do in intact ganglia, except that PTP does not occur in culture when sensory neurons are impaled. We measured spontaneous release 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 by an increase in mini frequency that decays with a time course parallel to the decay of evoked EPSP facilitation. In contrast, depression is not paralleled by a reduction of mini frequency, although extensive stimulation reduces mini frequency for a brief period immediately following stimulation. Neither form of plasticity altered miniature EPSP or miniature EPSC amplitude, corroborating previous evidence that both are presynaptically mediated. These findings suggest that PTP is mediated by a presynaptic mechanism independent of the action potential, such as vesicle mobilization. This presumably Ca(2+)- dependent mechanism does not involve protein kinase C, since we found that the inhibitor H7 does not specifically block PTP. In contrast to PTP, depression appears to involve changes unique to excitation- secretion coupling, such as reduced Ca2+ influx during the action potential (Klein et al., 1980).