Isoperiodic bursting by magnocellular neuroendocrine cells in the rat hypothalamic slice

1. Recruitment of magnocellular neuroendocrine cells (m.n.c.s) to a repetitive burst pattern (phasic firing) is associated with increased vasopressin secretion from neurohypophysial terminals in the intact animal. Based on invertebrate studies, bursts of action potentials can arise in two distinct ways: as an intrinsic property of the recorded cell or as an emergent property of synaptic interactions. 2. The majority of phasic m.n.c.s in the hypothalamic slice preparation display an endogenous pace-maker mechanism underlying bursting. It is voltage dependent and varies considerably in periodicity and time course as described in the accompanying paper (Andrew, 1987). 3. In contrast to this intrinsic mechanism, the present study examined if cells might be driven by periodic synaptic input. Intracellular recordings from six of thirty-two phasic m.n.c.s in the supraoptic nucleus revealed an isoperiodic oscillation of the membrane potential, where each depolarizing phase could support a burst. 4. The oscillation had a smooth trajectory and fixed period (range, 5-17 s). The oscillatory frequency was not voltage dependent, i.e. periodicity was unaffected by steady current injection through the recording electrode. 5. The frequency and amplitude of the oscillation remained unaltered by action potential firing. The isoperiodic oscillation could abate spontaneously, leaving intact the endogenous ability to fire a triggered burst driven by an underlying plateau potential. 6. Perfusion with either 10 mM-Mg2+-0.05 mM-Ca2+ or 0.5-2.0 microM-tetrodotoxin blocked both the oscillation and evoked post-synaptic potentials, indicating that the oscillation was synaptically generated. Given that both treatments could also block the intrinsic burst process and that the oscillation could spontaneously abate, the synaptic nature of the oscillation remains a tentative but reasonable conclusion. 7. In total, the evidence suggests that the isoperiodic oscillation has a synaptic origin independent of intrinsic mechanisms. It probably results from synaptic input generated within the slice but the source is not yet identified. This input could support phasic bursting in those m.n.c.s lacking a pace-maker ability and so promote the release of vasopressin in the intact animal.