REGULATION OF SYNAPTIC STRENGTH AT MIXED SYNAPSES - EFFECTS OF DOPAMINE-RECEPTOR BLOCKADE AND PROTEIN-KINASE-C ACTIVATION

Previous studies of the mixed excitatory synapses between eighth nerve afferents and the lateral dendrite of the goldfish Mauthner (M-) cell have shown that synaptic strength is enhanced for an hour or longer f ollowing either repeated brief tetanizations or local extracellular ap plications of dopamine. Both the initial electrotonic coupling potenti al, mediated via current flow through gap junctions, and the subsequen t chemically mediated excitatory postsynaptic potentials (EPSPs) are p otentiated. Different second messenger pathways are implicated in the postsynaptic induction of these potentiations, with a Ca2+ influx pres umably triggering the activity dependent long-term potentiations (LTP) and dopamine acting via a cAMP dependent pathway. Experiments perform ed to determine whether the LTP involves a stimulus-induced release of dopamine or requires a background level of dopamine receptor activati on suggest neither is the case, as tetanization in the presence of a D 1 receptor antagonist, which blocks the dopamine effects, produced an LTP comparable to that in the absence of the blocker. The effects of C a2+ are presumably not due to protein kinase C (PKC) activation, since phorbol esters had no effect on the mixed excitatory synaptic respons es, although they did enhance the frequency of spontaneously occurring inhibitory PSPs.