Egawa M, Yoshimatsu H, Bray G A
Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.
Am J Physiol. 1991 Feb;260(2 Pt 2):R328-34. doi: 10.1152/ajpregu.1991.260.2.R328.
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.
为了研究神经肽Y(NPY)对肩胛间棕色脂肪组织(IBAT)交感神经活动的影响,我们将NPY注入麻醉大鼠的第三脑室(icv)、视前内侧区(MPOA)、下丘脑前区(AHA)、下丘脑室旁核(PVN)、下丘脑腹内侧核(VMN)和下丘脑外侧区(LHA)。通过电生理学记录交感神经至IBAT的多单位放电。icv注射NPY以剂量依赖性方式抑制交感神经活动,随后逐渐恢复。向PVN单侧微量注射NPY(25 pmol)也显著抑制了至IBAT的交感神经活动。相反,向MPOA微量注射NPY显著增加了交感神经活动。向PVN或MPOA注射生理盐水对交感神经活动无显著影响。向AHA、VMN或LHA微量注射NPY(25 pmol)不会改变至IBAT的交感神经活动。我们得出结论,中枢给予NPY会影响至IBAT的交感神经活动,且NPY的抑制作用可能部分通过PVN起作用,该抑制作用比刺激作用更显著。这一结果与NPY是控制IBAT能量消耗的交感神经系统神经化学调节剂这一假设一致。