CA2-ACTIVATED K+ CHANNELS IN RAT OTIC GANGLION-CELLS - ROLE OF CA2+ ENTRY VIA CA2+ CHANNELS AND NICOTINIC RECEPTORS()

1. Intracellular recordings were made from neurones in the rat otic ga nglion in vitro in order to investigate their morphological, physiolog ical and synaptic properties. We took advantage of the simple structur e of these cells to test for a possible role of calcium influx via nic otinic acetylcholine receptors during synaptic transmission. 2. Cells filled with biocytin comprised a homogeneous population with ovoid som ata and sparse dendritic trees. Neurones had resting membrane potentia ls of -53 +/- 0.7 mV (n = 69), input resistances of 112 + 7 M Omega, a nd membrane time constants of 14 +/- 0.9 ms (n = 60). Upon depolarizat ion, all cells fired overshooting action potentials which mere followe d by an apamin-sensitive after-hyperpolarization (AHP). In response to a prolonged current injection, all neurones fired tonically. 3. The r epolarization phase of action potentials had a calcium component which was mediated by N-type calcium channels. Application of omega-conotox in abolished both the repolarizing hump and the after-hgrperpolarizati on suggesting that calcium influx via N-type channels activates SK-typ e calcium-activated potassium channels which underlie the AHP. 4. The majority (70%) of neurones received innervation from a single pregangl ionic fibre which generated a suprathreshold excitatory postsynaptic p otential mediated by nicotinic acetylcholine receptors. The other 30% of neurones also had one or more subthreshold nicotinic inputs. 5. Cal cium influx via synaptic nicotinic receptors contributed to the AHP cu rrent, indicating that this calcium has access to the calcium-activate d potassium channels and therefore plays a role in regulating cell exc itability.