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Peer-reviewed veterinary case report

Neurophysiology of supraoptic neurons in C57/BL mice studied in three acute in vitro preparations.

Journal:
Progress in brain research
Year:
2008
Authors:
Sharif-Naeini, Reza et al.
Affiliation:
Montreal General Hospital and McGill University · Canada
Species:
rodent

Abstract

Osmotic control of arginine vasopressin (AVP) and oxytocin (OXT) release from magnocellular neurosecretory cells (MNCs) of the supraoptic (SON) and paraventricular (PVN) nuclei is essential for body fluid homeostasis. The electrical activity of MNCs, which is regulated by intrinsic and extrinsic osmosensitive factors, is a primary determinant of blood AVP and OXT levels. Although we now understand many of the cellular mechanisms that mediate the osmotic control of electrical activity and secretion from MNCs, further insight is likely to emerge from a molecular analysis of these mechanisms. An important step towards this goal could be made through the use of mouse genetic models. However, the electrophysiological properties of MNCs in mice have not been characterized, making direct comparisons with the rat model somewhat difficult. In this study, we examined the electrical properties of MNCs from the mouse SON. Extracellular recordings from neurons in superfused explants revealed modes of basal and osmotically modulated firing very similar to those observed previously in rats. Recordings in hypothalamic slices confirmed that SON neurons receive kynurenic-acid-sensitive excitatory synaptic inputs from the organum vasculosum laminae terminalis (OVLT). Current-clamp recordings from acutely dissociated SON neurons showed proportional changes in membrane cation conductance during changes in fluid osmolality. We conclude, therefore, that MNCs in the mouse SON display intrinsic osmosensitive properties and firing patterns that are very similar to those reported in the rat. Mouse MNCs therefore represent a useful model for the study of molecular factors contributing to the osmotic control of AVP and OXT release.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/18655886/