Electrophysiological characteristics of immunochemically identified rat oxytocin and vasopressin neurones in vitro.
1. Intracellular recordings were made from supraoptic neurones in vitro from hypothalamic explants prepared from adult male rats. Neurones were injected with biotinylated markers, and of thirty-nine labelled neurones, nineteen were identified immunocytochemically as containing oxytocin-neurophysin and twenty as containing vasopressin-neurophysin. 2. Vasopressin and oxytocin neurones did not differ in their resting membrane potential, input resistance, membrane time constant, action potential height from threshold, action potential width at half-amplitude, and spike hyperpolarizing after-potential amplitude. Both cell types exhibited spike broadening during brief, evoked spike trains (6-8 spikes), but the degree of broadening was slightly greater for vasopressin neurones. When hyperpolarized below -75 mV, all but one neurone exhibited a transient outward rectification to depolarizing pulses, which delayed the occurrence of the first spike. 3. Both cell types exhibited a long after-hyperpolarizing potential (AHP) following brief spike trains evoked either with a square wave pulse or using 5 ms pulses in a train. There were no significant differences between cell types in the size of the AHP evoked with nine spikes, or in the time constant of its decay. The maximal AHP evoked by a 180 ms pulse was elicited by an average of twelve to thirteen spikes, and neither the size of this maximal AHP nor its time constant of decay were different for the two cell types. 4. In most oxytocin and vasopressin neurones the AHP, and concomitantly spike frequency adaptation, were markedly reduced by the bee venom apamin and by d-tubocurarine, known blockers of a Ca(2+)-mediated K+ conductance. However, a minority of neurones, of both cell types, were relatively resistant to both agents. 5. In untreated neurones, 55% of vasopressin neurones and 32% of oxytocin neurones exhibited a depolarizing after-potential (DAP) after individual spikes or, more commonly, after brief trains of spikes evoked with current pulses. For each neurone with a DAP, bursts of spikes could be evoked if the membrane potential was sufficiently depolarized such that the DAP reached spike threshold. In four out of five vasopressin neurones a DAP became evident only after pharmacological blockade of the AHP, whereas in six oxytocin neurones tested no such masking was found. 6. The firing patterns of neurones were examined at rest and after varying the membrane potential with continuous current injection. No identifying pattern was strictly associated with either cell type, and a substantial number of neurones were silent at rest.(ABSTRACT TRUNCATED AT 400 WORDS)
Armstrong
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WE
Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163.
Smith
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BN
Tian
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D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001710:Biotin / Q000031:analogs & derivatives; D002462:Cell Membrane / Q000502:physiology; D004594:Electrophysiology; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008239:Lysine / Q000031:analogs & derivatives; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009474:Neurons / Q000378:metabolism / Q000502:physiology*; D010121:Oxytocin / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013495:Supraoptic Nucleus / Q000166:cytology / Q000378:metabolism; D014403:Tubocurarine / Q000494:pharmacology; D014667:Vasopressins / Q000502:physiology*
C070614:neurobiotin; D014667:Vasopressins; D001030:Apamin; D010121:Oxytocin; D001710:Biotin; C013411:biocytin; D008239:Lysine; D014403:Tubocurarine