Endogenous bursting by rat supraoptic neuroendocrine cells is calcium dependent.

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Abstract
1. Phasic bursting by magnocellular neuroendocrine cells (m.n.c.s) in vivo causes increased vasopressin release from axon terminals in the neurohypophysis. In the supraoptic nucleus of the coronal hypothalamic slice thirty-two of sixty-five m.n.c.s recorded intracellularly displayed repetitive bursting, either spontaneously or during a low level of tonic current injection. 2. Of the thirty-two repetitive bursters, twenty-four received no apparent patterned synaptic input and the phasic burst behavior was voltage dependent. The evidence for these cells being bursting pace-makers and the underlying mechanism driving bursting were further investigated. 3. Phasic bursting by m.n.c.s is usually contingent upon two depolarizing events: a slow depolarization (s.d.) between bursts that brings the membrane potential to burst threshold, and the spike depolarizing after-potential (d.a.p.). One or several d.a.p.s can initiate a burst by summing to form a plateau potential which sustains firing. 4. Of eight phasic cells exposed to tetrodotoxin (TTX) and tonically depolarized with current injection, two cells retained the phasic burst pattern and underlying plateau potentials. Of the remaining six cells in TTX, three of four cells tested regained phasic firing with plateau potentials following the addition of Sr2+, a Ca2+ agonist. Evoked post-synaptic potentials were demonstrably blocked throughout TTX exposure, firmly establishing that some m.n.c.s are bursting pace-makers. 5. The s.d., d.a.p. and plateau potential were retained in TTX or low-Na+ saline, augmented in Sr2+ and blocked in low-Ca2+ saline. All three events were activated at membrane potentials depolarized from -70 mV but steadily inactivated with increasing hyperpolarization to -90 mV. The s.d. and d.a.p. apparently represented partial activation of the same process that drives a burst, the plateau potential. 6. Hyperpolarizing pulses of constant current revealed an apparent decrease in cell conductance underlying the s.d., d.a.p. and plateau potential which was not due to membrane rectification. The plateau potential was reduced in low Na+ and eliminated in low Ca2+. However, it remained relatively unaffected by altering the external K+ concentration and it did not reverse below -90 mV, suggesting a less important role for K+ movement relative to Ca2+ or Na+. A hyperpolarizing pulse during the s.d., d.a.p. or plateau potential probably momentarily inactivated inward Ca2+ current, causing the apparent conductance decrease. 7. In total, the findings suggest that Ca2+ influx is prerequisite for generation of the s.d., d.a.p. and plateau potential and thus for intrinsic phasic firing. Hypothetically, a slow intracellular accumulation of Ca2+ during each burst might reduce inward Ca2+ current, leading to the subsequent interburst period. 8. The variable activation and inactivation rates of the s.d. plateau potential explains why phasic firing by m.n.c.s usually fluctuates considerably in periodicity from burst to burst. Where periodicity is fixed, another mechanism is responsible, as examined in the accompanying paper (Andrew, 1987).