Intracellular study of calcium‐related events in cat magnocellular neuroendocrine cells.

1. Magnocellular neuroendocrine cells (MNCs) in the supraoptic nucleus (SON) of mammals synthesize vasopressin or oxytocin and release these hormones systemically from their neurohypophysial axon terminals. In the rat, release is facilitated by bursts of action potentials generated by the MNC. However MNC units in the intact cat discharge more slowly and do not display the repetitive bursts (phasic firing) that promote vasopressin secretion. The reasons why these cat endocrine neurones differ so dramatically in their firing behaviour from the rat model were examined using intracellular recording. 2. Cat and rat MNCs displayed similar mean resting potentials approximating ‐60 mV, and were usually linear in their voltage‐current relationship in the hyperpolarizing direction. However cat MNCs displayed a higher mean cell input resistance (301 M omega; n = 56) than those of rat (150 M omega; n = 105). 3. Calcium influx to cat MNCs during firing appeared comparable to rat based on (a) the similar range of action potential broadening observed during a spike train, (b) the shoulder on the action potential's falling phase which was blocked in low‐Ca2+ saline, and (c) the ability to evoke tetrodotoxin (TTX)‐insensitive spiking and non‐synaptic depolarizing potentials, both calcium‐mediated events observed in the rat. 4. In cat MNCs, a depolarizing current pulse (100‐500 ms; 0.1‐0.3 nA) elicited a train of action potentials followed by a prominent after‐hyperpolarization (AHP) several times the duration of its counterpart in the rat. The AHP reversed near the equilibrium potential for K+, was not voltage dependent and represented an increased membrane conductance. It was suppressed in low‐Ca2+ saline and completely eliminated by the calcium‐activated potassium current (IK(Ca)) blockers apamin (100 nM) or d‐tubocurarine (50‐200 microM). Both blockers decreased spike frequency adaptation but did not induce bursting. Therefore the cat AHP probably represents a Ca(2+)‐activated K+ conductance with a similar blocker sensitivity to its briefer counterpart in the rat MNC. 5. The spike hyperpolarizing after‐potentials (HAPs) in cat were more than twice the mean amplitude and several times the duration of HAPs in rat. Cat HAPs were qualitatively similar to their rat counterparts, remaining unaffected by apamin or tubocurarine. The intrinsic currents responsible for the AHP and HAP appear to generate the stronger activity‐dependent inhibition displayed by cat MNCs. 6. Twenty‐one of fifty‐two cat MNCs displayed an inward rectification at membrane potentials more negative than ‐70 mV ([K+]o = 6.24 mM), causing a depolarizing 'sag' in the voltage trajectory lasting 100‐200 ms which was TTX resistant.(ABSTRACT TRUNCATED AT 400 WORDS)