RT Journal Article
SR Electronic
T1 Modulation of spontaneous transmitter release during depression and posttetanic potentiation of Aplysia sensory-motor neuron synapses isolated in culture
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 3280
OP 3292
DO 10.1523/JNEUROSCI.14-05-03280.1994
VO 14
IS 5
A1 LS Eliot
A1 ER Kandel
A1 RD Hawkins
YR 1994
UL http://www.jneurosci.org/content/14/5/3280.abstract
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).