title: Opioids potentiate electrical transmission at mixed synapses on the Mauthner cell.
abstract: Opioid receptors were shown to modulate a variety of cellular processes in the vertebrate central nervous system, including synaptic transmission. While the effects of opioid receptors on chemically mediated transmission have been extensively investigated, little is known of their actions on gap junction-mediated electrical synapses. Here we report that pharmacological activation of mu-opioid receptors led to a long-term enhancement of electrical (and glutamatergic) transmission at identifiable mixed synapses on the goldfish Mauthner cells. The effect also required activation of both dopamine D1/5 receptors and postsynaptic cAMP-dependent protein kinase A, suggesting that opioid-evoked actions are mediated indirectly via the release of dopamine from varicosities known to be located in the vicinity of the synaptic contacts. Moreover, inhibitory inputs situated in the immediate vicinity of these excitatory synapses on the lateral dendrite of the Mauthner cell were not affected by activation of mu-opioid receptors, indicating that their actions are restricted to electrical and glutamatergic transmissions co-existing at mixed contacts. Thus, as their chemical counterparts, electrical synapses can be a target for the modulatory actions of the opioid system. Because gap junctions at these mixed synapses are formed by fish homologs of the neuronal connexin 36, which is widespread in mammalian brain, it is likely that this regulatory property applies to electrical synapses elsewhere as well.
authors.affiliation: Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York; and.
authors.forename: Roger
authors.initials: R
authors.lastname: Cachope
authors.affiliation: Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York; and Marine Biological Laboratory, Woods Hole, Massachusetts alberto.pereda@einstein.yu.edu.
authors.forename: Alberto E
authors.initials: AE
authors.lastname: Pereda
mesh_terms: D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D018492:Dopamine Antagonists / Q000494:pharmacology; D004558:Electric Stimulation; D054351:Electrical Synapses / Q000187:drug effects* / Q000502:physiology; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000494:pharmacology*; D029941:Fish Proteins / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006054:Goldfish; D008839:Microelectrodes; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors / Q000378:metabolism; D050641:Receptors, Dopamine D5 / Q000378:metabolism; D013116:Spinal Cord / Q000502:physiology
chemical_list: D000701:Analgesics, Opioid; D001552:Benzazepines; D018492:Dopamine Antagonists; D029941:Fish Proteins; D009292:Narcotic Antagonists; D017447:Receptors, Dopamine D1; C534628:SCH 23390; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D050641:Receptors, Dopamine D5; D009270:Naloxone; D018698:Glutamic Acid; D017868:Cyclic AMP-Dependent Protein Kinases; D004298:Dopamine
keywords: Mauthner cell; auditory; connexin 35; connexin 36; dopamine; gap junction; teleost