Synaptic activation of phasic bursting in rat supraoptic nucleus neurones recorded in hypothalamic slices.
Using slices of rat hypothalamus (400-500 micron thick), intracellular and extracellular recordings were made of activity from eight-eight neurones in the supraoptic nucleus (s.o.n.). Electrical stimulation with single stimuli dorsolateral to s.o.n. was excitatory to fifty-nine 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 s.o.n. did not evoke responses. Stimulation dorsomedial to the nucleus produced only direct, probably antidromic, activation of s.o.n. neurones. Application of acetylcholine (ACh) by microperifusion in the s.o.n. region mimicked the effect of electrical stimulation by evoking prolonged discharge in eight of eight tested phasically firing s.o.n. neurones. Non-phasic, continuously firing neurones were either inhibited or unaffected by electrical stimulation in the critical region. The discharge pattern of unaffected cells (six 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 dorso-lateral region were blocked reversibly by the nicotinic blockers, d-tubocurarine chloride and hexamethonium bromide (in seven of seven cells tested), but were unaffected by the muscarinic blocker, atropine, even at high concentrations (two of two cells tested). Thus, this activation appears to be mediated by nicotinic receptors. In separate experiments with the position of stimulating and recording electrodes reversed, s.o.n. stimulation was effective in antidromically activating one cell of sixty-eight recorded extracellularly in the dorsolateral region. Some slowly firing s.o.n. neurones (less than 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 i.p.s.p.s. and/or inhibition of ongoing activity for the duration of the stimulus train. These results support evidence from earlier studies that the cholinergic input to s.o.n. neurones originates from cells in its close proximity, and suggests this input to be via a monosynaptic pathway.
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D005071:Evoked Potentials / Q000187:drug effects; D006584:Hexamethonium Compounds / Q000494:pharmacology; D066298:In Vitro Techniques; D009474:Neurons / Q000502:physiology*; D051381:Rats; D013495:Supraoptic Nucleus / Q000166:cytology*; D013569:Synapses / Q000502:physiology*; D013997:Time Factors; D014403:Tubocurarine / Q000494:pharmacology
D006584:Hexamethonium Compounds; D001285:Atropine; D000109:Acetylcholine; D014403:Tubocurarine