Murugaiah K D, O'Donnell J M
Department of Pharmacology and Therapeutics, Louisiana State University Medical School, Shreveport 71130, USA.
Res Commun Mol Pathol Pharmacol. 1995 Nov;90(2):179-90.
Basal and electrical stimulation-induced release of tritiated norepinephrine (3H-NE) was determined in superfused slices of the rat hypothalamus and hippocampus. Isoproterenol (0.1-10 nM), a nonselective beta-adrenergic agonist, enhanced stimulation-evoked release of 3H-NE from hypothalamic and hippocampal slices in a concentration-dependent manner without consistently altering basal release. Isoproterenol (1 nM) increased ratios of S2/S1 to 143 +/- 4% (hypothalamus) and 152 +/- 15% (hippocampus) of control values. The facilitatory effects of isoproterenol were antagonized by propranolol (50 nM), a nonselective beta-adrenergic antagonist. The beta 2-selective adrenergic agonist clenbuterol (10-100 microM) enhanced basal release of 3H-NE in a concentration-dependent fashion. These results provide evidence for a beta-adrenergic receptor mediated regulation of NE release from hypothalamic and hippocampal slices. Whether the positive feedback mechanism contributes to any of the NE-mediated physiological functions associated with the hypothalamus and hippocampus requires further study. However, the effect of clenbuterol indicates that some of its behavioral actions in animals may be attributed to this NE release-enhancing effect observed in the present study.
在大鼠下丘脑和海马的灌流切片中测定了基础状态及电刺激诱导的氚标记去甲肾上腺素(3H-NE)释放。异丙肾上腺素(0.1 - 10 nM),一种非选择性β-肾上腺素能激动剂,以浓度依赖性方式增强了下丘脑和海马切片中电刺激诱发的3H-NE释放,且未持续改变基础释放量。异丙肾上腺素(1 nM)使S2/S1比值增加至对照值的143±4%(下丘脑)和152±15%(海马)。异丙肾上腺素的促进作用被非选择性β-肾上腺素能拮抗剂普萘洛尔(50 nM)拮抗。β2选择性肾上腺素能激动剂克伦特罗(10 - 100 μM)以浓度依赖性方式增强了3H-NE的基础释放。这些结果为β-肾上腺素能受体介导的下丘脑和海马切片中NE释放的调节提供了证据。这种正反馈机制是否有助于与下丘脑和海马相关的任何NE介导的生理功能,还需要进一步研究。然而,克伦特罗的作用表明其在动物中的一些行为效应可能归因于本研究中观察到的这种NE释放增强作用。