Regulation of synaptic strength at mixed synapses: Effects of dopamine receptor blockade and protein kinase C activation

A. Silva, S. Kumar, A. Pereda, D. S. Faber

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


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 following either repeated brief tetanizations or local extracellular applications of dopamine. Both the initial electrotonic coupling potential, mediated via current flow through gap junctions, and the subsequent chemically mediated excitatory postsynaptic potentials (EPSPs) are potentiated. Different second messenger pathways are implicated in the postsynaptic induction of these potentiations, with a Ca2+ influx presumably triggering the activity dependent long-term potentiations (LTP) and dopamine acting via a cAMP dependent pathway. Experiments performed to determine whether the LTP involves a stimulus-induced release of dopamine or requires a background level of dopamine receptor activation suggest neither is the case, as tetanization in the presence of a D1 receptor antagonist, which blocks the dopamine effects, produced an LTP comparable to that in the absence of the blocker. The effects of Ca2+ are presumably not due to protein kinase C (PKC) activation, since phorbol esters had no effect on the mixed excitatory synaptic responses, although they did enhance the frequency of spontaneously occurring inhibitory PSPs.

Original languageEnglish (US)
Pages (from-to)1559-1565
Number of pages7
Issue number11
StatePublished - Nov 1995
Externally publishedYes


  • Mauthner cell
  • calcium
  • dopamine
  • gap junctions
  • long-term potentiation
  • protein kinase C

ASJC Scopus subject areas

  • Pharmacology
  • Cellular and Molecular Neuroscience


Dive into the research topics of 'Regulation of synaptic strength at mixed synapses: Effects of dopamine receptor blockade and protein kinase C activation'. Together they form a unique fingerprint.

Cite this