Neuropeptide Y suppresses sympathetic activity to interscapular brown adipose tissue in rats

M Egawa, H Yoshimatsu… - American Journal of …, 1991 - journals.physiology.org
M Egawa, H Yoshimatsu, GA Bray
American Journal of Physiology-Regulatory, Integrative and …, 1991journals.physiology.org
To investigate the effects of neuropeptide Y (NPY) on sympathetic nerve activity to
interscapular brown adipose tissue (IBAT), we injected NPY into the third cerebroventricle
(icv), medial preoptic area (MPOA), anterior hypothalamic area (AHA), paraventricular
hypothalamic nucleus (PVN), ventromedial hypothalamic nucleus (VMN), and lateral
hypothalamic area (LHA) of anesthetized rats. Multiunit discharges from sympathetic nerves
to IBAT were recorded electrophysiologically. The icv injection of NPY suppressed …
To investigate the effects of neuropeptide Y (NPY) on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), we injected NPY into the third cerebroventricle (icv), medial preoptic area (MPOA), anterior hypothalamic area (AHA), paraventricular hypothalamic nucleus (PVN), ventromedial hypothalamic nucleus (VMN), and lateral hypothalamic area (LHA) of anesthetized rats. Multiunit discharges from sympathetic nerves to IBAT were recorded electrophysiologically. The icv injection of NPY suppressed sympathetic nerve activity in a dose-dependent manner, followed by a gradual recovery. The microinjection of NPY (25 pmol) unilaterally into the PVN also significantly suppressed the sympathetic nerve activity to IBAT. In contrast, microinjection of NPY into the MPOA significantly increased the sympathetic nerve activity. The injection of saline into either the PVN or MPOA had no significant effect on sympathetic nerve activity. The microinjection of NPY (25 pmol) into the AHA, VMN, or LHA did not change sympathetic nerve activity to IBAT. We conclude that central administration of NPY affects the sympathetic nerve activity to IBAT and that the suppressive effect of NPY, which may act in part through the PVN, is dominant to the stimulatory effect. The result is consistent with the hypothesis that NPY is a neurochemical modulator of the sympathetic nervous system which controls energy expenditure in IBAT.
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