SYNAPTIC PLASTICITY IN THE CEREBRAL GANGLION OF APLYSIA

The A-B neuron synapses in the cerebral ganglion of Aplysia exhibit tw o prominent forms of activity-dependent plasticity. Stimulating indivi dual presynaptic A neurons at low frequencies (0.002-5 Hz) causes syna ptic depression of EPSPs and EPSCs in postsynaptic B neurons, while te tanizing A neurons with 4,500 ms trains of 35 ms pulses at 20 Hz evoke s a long-lasting (similar to 25 min) increase in EPSP amplitudes. Due to its slow kinetics, we have called this latter plasticity slow devel oping potentiation (SDP). Both depression and SDP are neuron-specific. Several lines of evidence support the hypothesis that SDP has a presy naptic locus. SDP can be induced while voltage clamping the postsynapt ic neuron. There are no changes in either input resistance or the stea dy-state I-V curve of B neurons during SDP. SDP does not require depol arization and spiking by the postsynaptic neuron. Pairing pre- and pos tsynaptic tetanization fails to increase SDP. Additionally, the revers al potential of the control and potentiated EPSCs are essentially the same (+ 11-12 mV). In contrast, there is a significant reduction in to tal outward current in the presynaptic A neurons following the tetaniz ation. However, SDP does not appear to be due to the inactivation of a steady-state Kf current. SDP may be in part mediated by PKC. PKC acti vators enhance SDP, while injecting the peptide inhibitor PKC19-36 blo cks it. Both Ca2+ entry, antagonized by L-channel blockers and ryanodi ne-sensitive release of Ca2+ from internal stores appear to contribute to SDP. Using quantal analysis, three independent measures indicate t hat SDP is due to increased quantal content. All these changes are con sistent with an SDP requiring an increase in intracellular Ca2+, leadi ng to increased transmitter release and a primary, if not exclusive, p resynaptic locus for the observed synaptic plasticity.