title: Neurotransmitter modulation of gap junctional communication in the rat hippocampus.
abstract: Increasing experimental evidence indicates that gap junctions can be modulated by neurotransmitters, in particular dopamine. To examine possible modulation of gap junctional communication in the rat hippocampus by neurotransmitters, we studied dye coupling and electrotonic transmission in the CA1 area in the presence of carbachol, a cholinergic agonist, and dopamine agonists. Carbachol markedly reduced dye coupling and the frequency of electrotonic potentials (spikelets). Spikelet amplitudes were decreased in the presence of carbachol. These effects were reversed by the cholinergic antagonist atropine, suggesting a muscarinic action of carbachol on gap junctional function. The non-specific dopamine agonist apomorphine, and the specific D1 receptor agonist SKF 38393, reduced dye coupling between pyramidal cells. Spikelet frequency was also decreased in the presence of dopamine agonists, but less than with carbachol. The specific D1 receptor antagonist, SCH 23390, reversed the effects of both dopamine agonists. These observations indicate that cholinergic and dopaminergic transmission can affect electrical and chemical (dye coupling) communication through gap junctions, and could therefore alter properties of neuronal assemblies, in addition to their effects on intrinsic membrane properties.
authors.affiliation: Toronto Hospital Research Institute, Department of Physiology, University of Toronto, Ontario, Canada.
authors.forename: J L
authors.initials: JL
authors.lastname: Velazquez
authors.forename: D
authors.initials: D
authors.lastname: Han
authors.forename: P L
authors.initials: PL
authors.lastname: Carlen
mesh_terms: D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D002450:Cell Communication / Q000187:drug effects / Q000502:physiology*; D002799:Cholinergic Fibers / Q000502:physiology; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D005456:Fluorescent Dyes / Q000493:pharmacokinetics; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology*; D006624:Hippocampus / Q000166:cytology* / Q000378:metabolism; D007546:Isoquinolines / Q000493:pharmacokinetics; D009474:Neurons / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D018377:Neurotransmitter Agents / Q000378:metabolism* / Q000502:physiology*; D010276:Parasympatholytics / Q000494:pharmacology; D010277:Parasympathomimetics / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017447:Receptors, Dopamine D1 / Q000819:agonists / Q000037:antagonists & inhibitors
chemical_list: D001552:Benzazepines; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D005456:Fluorescent Dyes; D007546:Isoquinolines; D018377:Neurotransmitter Agents; D010276:Parasympatholytics; D010277:Parasympathomimetics; D017447:Receptors, Dopamine D1; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; D001285:Atropine; D002217:Carbachol; C017475:lucifer yellow; D001058:Apomorphine