Dopamine enhances both electrotonic coupling and chemical excitatory postsynaptic potentials at mixed synapses

Alberto Pereda, Antoine Triller, Henri Korn, Donald S. Faber

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

The transmitter dopamine reduces electrotonic coupling between retinal horizontal cells and increases their sensitivity to glutamate. Since in other systems single afferents establish mixed electrotonic and chemical excitatory synapses with their targets, dopamine might be expected there to depress one component of excitation while enhancing the other. This hypothesis was tested by applying dopamine locally in the vicinity of the lateral dendrite of the goldfish Mauthner cell (M cell) and monitoring the composite electrotonic and chemical excitatory postsynaptic potentials and currents evoked by ipsilateral eighth nerve stimulation. Dopamine produces persistent enhancements of both components of the postsynaptic response while it also increases input conductance. All these dopamine actions are prevented by superfusing the brain with saline containing the dopamine D1 receptor antagonist SCH-23390. Postsynaptic injections of the cAMP-dependent protein kinase inhibitor (Walsh inhibitor, or PKI5-24) block the dopamine-induced changes in synaptic transmission, implicating a cAMP-dependent mechanism. Furthermore, there is a dopaminergic innervation of the M cell, as demonstrated immunohistochemically with antibodies against dopamine and the rate-limiting enzyme in its synthetic pathway, tyrosine hydroxylase. Varicose immunoreactive fibers lie in the vicinity of the distal part of the lateral dendrite between the large myelinated club endings that establish the mixed synapses. As determined with electron microscopy, the dopaminergic fibers contain small vesicles, and they do not have synaptic contacts with either the afferents or the M cell, remaining instead in the synaptic bed. Taken together, these results suggest that dopamine released at a distance from these terminals increases the gain of this primary sensory input to the M cell, most likely through a phosphorylation mechanism.

Original languageEnglish (US)
Pages (from-to)12088-12092
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume89
Issue number24
DOIs
StatePublished - Jan 1 1992
Externally publishedYes

Keywords

  • Gap junctions
  • Long-term enhancement
  • Mauthner cell

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Dopamine enhances both electrotonic coupling and chemical excitatory postsynaptic potentials at mixed synapses'. Together they form a unique fingerprint.

  • Cite this