Synaptic activation of phasic bursting in rat supraoptic nucleus neurones recorded in hypothalamic slices.

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Abstract
Using slices of rat hypothalamus (400-500 .mu.m thick), intracellular and extracellular recordings were made of activity from 88 neurons in the supraoptic nucleus(SON). Electrical stimulation with single stimuli dorsolateral to SON was excitatory 59 phasically firing cells (67% of total, 95% of phasic cells). In intracellularly recorded cells, such stimulation reliably evoked excitatory post-synaptic potentials which often gave rise to action potentials. Trains of stimuli reliably triggered bursts of action potentials which continued after stimulation had ceased. Stimulation more dorsal or more lateral to the critical region or in the optic tract adjacent to the SON did not evoke responses. Stimulation dorsomedial to the nucleus produced only direct, probably antidromic, activation of SON neurons. Application of acetylcholine (ACh) by microperifusion in the SON region mimicked the effect of electrical stimulation by evoking prolonged discharge in 8 of 8 tested phasically firing SON neurons. Non-phasic, continuously firing neurons were either inhibited or unaffected by electrical stimulation in the critical region. The discharge pattern of unaffected cells (6 cells) was not modified by locally applied ACh, although they were excited by local application of sodium glutamate. The excitatory, synaptically mediated, responses to stimulation in the dorsolateral region were blocked reversibly by the nicotinic blockers, d-tubocurarine chloride and hexamethonium bromide (in 7 of 7 cells tested), but were unaffected by the muscarinic blocker, atropine, even at high concentrations (2 of 2 cells tested). This activation appears to be mediated by nicotinic receptors. In separate experiments with the position of stimulating and recording electrodes reversed, SON stimulation was effective in antidromically activating 1 cell of 68 recorded extracellulary in the dorsolateral region. Some slowly firing SON neurons (< 4 Hz) were inhibited by electrical stimulation in the same area in which phasically active cells were excited. In these cases, stimulation produced large summating IPSP [inhibitory postsynaptic potential] and/or inhibition of ongoing activity for the duration of the stimulus train. The cholinergic input to SON neurons originates from cells in its close proximity, and suggests this input to be via a monosynaptic pathway.