Intrinsic Inhibition in Magnocellular Neuroendocrine Cells of Rat Hypothalamus

Overview

Journal J Physiol

Specialty Physiology

Date 1984 Aug 1

PMID 6090639

Citations 42

Authors

R D Andrew

F E Dudek

Affiliations

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Abstract

Endogenous mechanisms of inhibition in magnocellular neuroendocrine cells were studied with intracellular recordings in the rat hypothalamic slice preparation. Hyperpolarizing after-potentials (duration up to 125 ms) followed single action potentials and after-hyperpolarizations (a.h.p.s) lasting hundreds of milliseconds followed brief evoked spike trains. The amplitude and duration of the a.h.p. increased after spike trains of longer duration or higher frequency. The a.h.p. appears endogenous, rather than synaptically mediated from recurrent inhibition, because it persisted after pharmacological blockade of axonal conduction or of chemical synaptic transmission. The reversal potential of the a.h.p. was at least 20 mV more negative than that of inhibitory post-synaptic potentials. Cl- ionophoresis did not alter the a.h.p. Chelation of intracellular Ca2+ with EGTA injection eliminated the a.h.p. A Ca2+-activated K+ conductance, rather than recurrent synaptic inhibition, apparently causes the a.h.p. and is at least partly responsible for the inhibition after single spikes in magnocellular neurones. During hormone release, this endogenous mechanism may contribute to the post-burst silent period in putative oxytocinergic cells and to the interburst interval in phasic neurones, which are known to fire repetitive bursts associated with vasopressin release.

Citing Articles

Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.

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Phasic spiking in vasopressin neurons: How and Why.

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Specificity in the interaction of high-voltage-activated Ca channel types with Ca-dependent afterhyperpolarizations in magnocellular supraoptic neurons.

Kirchner M, Foehring R, Callaway J, Armstrong W J Neurophysiol. 2018; 120(4):1728-1739.

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A reduction in SK channels contributes to increased activity of hypothalamic magnocellular neurons during heart failure.

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Leng T, Leng G, MacGregor D PLoS One. 2017; 12(7):e0180368.

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