NEUROTRANSMITTER MODULATION OF GAP JUNCTIONAL COMMUNICATION IN THE RAT HIPPOCAMPUS

Increasing experimental evidence indicates that gap junctions can be m odulated by neurotransmitters, in particular dopamine. To examine poss ible modulation of gap junctional communication in the rat hippocampus by neurotransmitters, we studied dye coupling and electrotonic transm ission in the CA1 area in the presence of carbachol, a cholinergic ago nist, and dopamine agonists. Carbachol markedly reduced dye coupling a nd the frequency of electrotonic potentials (spikelets). Spikelet ampl itudes were decreased in the presence of carbachol. These effects were reversed by the cholinergic antagonist atropine, suggesting a muscari nic action of carbachol on gap junctional function. The non-specific d opamine agonist apomorphine, and the specific D-1 receptor agonist SKF 38393, reduced dye coupling between pyramidal cells. Spikelet frequen cy was also decreased in the presence of dopamine agonists, but less t han with carbachol. The specific D, receptor antagonist, SCH 23390, re versed the effects of both dopamine agonists. These observations indic ate that cholinergic and dopaminergic transmission can affect electric al and chemical (dye coupling) communication through gap junctions, an d could therefore alter properties of neuronal assemblies, in addition to their effects on intrinsic membrane properties.