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Volume 16, Number 23, Issue of December 1, 1996 pp. 7526-7532
Copyright ©1996 Society for Neuroscience

Atrial Natriuretic Peptide Modulates Synaptic Transmission from Osmoreceptor Afferents to the Supraoptic Nucleus

Received Aug. 25, 1996; revised Sept. 17, 1996; accepted Sept. 18, 1996.

Dominique Richard and Charles W. Bourque

Centre for Research in Neuroscience, Montreal General Hospital Research Institute and McGill University, Montréal, Québec, Canada H3G 1A4

Atrial natriuretic peptide (ANP) and its receptors are present in hypothalamic nuclei containing the magnocellular neurosecretory cells (MNCs), which release vasopressin and oxytocin. In the rat, intracerebroventricular injections of ANP inhibit the release of both hormones in response to hypertonicity. Although these findings suggest a role for endogenous ANP in the central control of fluid balance, cellular mechanisms underlying the modulatory actions of ANP are unknown. We therefore examined the effects of ANP on the osmoresponsiveness of MNCs impaled in rat hypothalamic explants. Applications of ANP (75-150 nM) over the supraoptic nucleus did not affect depolarizing responses to local hypertonicity, but they reversibly abolished the synaptic excitation of MNCs after hypertonic stimulation of the organum vasculosum laminae terminalis (OVLT). These effects were associated with decreased spontaneous EPSP (sEPSP) amplitude rather than with changes in sEPSP frequency. Accordingly, application of ANP reduced the amplitude of glutamatergic EPSPs evoked by electrical stimulation of the OVLT (IC₅₀ ~ 3 nM). The inhibitory effects of ANP on EPSP amplitude were mimicked by application of 3-5-dibutyryl cGMP, consistent with the guanylate cyclase activity of natriuretic peptide receptors. Although depolarizing responses of MNCs to ionotropic glutamate receptor agonists were unaffected by ANP, the peptide reversibly enhanced paired-pulse facilitation of electrically evoked EPSPs. These results indicate that centrally released ANP may inhibit osmotically evoked neurohypophysial hormone release through presynaptic inhibition of glutamate release from osmoreceptor afferents derived from the OVLT.

Key words: atrial natriuretic peptide; supraoptic nucleus; OVLT; organum vasculosum lamina terminalis; osmoregulation; vasopressin; oxytocin; osmoreceptor; presynaptic inhibition

This article has been cited by other articles:

				J. ANTUNES-RODRIGUES, M. DE CASTRO, L. L. K. ELIAS, M. M. VALENCA, and S. M. McCANN Neuroendocrine Control of Body Fluid Metabolism Physiol Rev, January 1, 2004; 84(1): 169 - 208. [Abstract] [Full Text] [PDF]

				M Hirasawa, S B Kombian, and Q J Pittman Oxytocin retrogradely inhibits evoked, but not miniature, EPSCs in the rat supraoptic nucleus: role of N- and P/Q-type calcium channels J. Physiol., May 1, 2001; 532(3): 595 - 607. [Abstract] [Full Text] [PDF]

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