用17-β雌二醇进行短期治疗可增强培养的大鼠结节漏斗神经元的自发性[3H]多巴胺释放。

Short-term treatment with 17-beta estradiol enhances spontaneous [3H] dopamine release from cultured rat tuberoinfundibular neurons.

作者信息

Yamaguchi M, Koike K, Kadowaki K, Miyake A, Tanizawa O

机构信息

Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.

出版信息

J Endocrinol Invest. 1991 Mar;14(3):187-91. doi: 10.1007/BF03346785.

DOI:10.1007/BF03346785

PMID:2071821

Abstract

The effects of 17-beta estradiol (E2) on spontaneous [3H] dopamine ([3H]DA) release was investigated using primary cultured cells from the tuberoinfundibular region of rat hypothalamus, which includes DA neurons. [3H] DA uptake by the neurons in the presence of E2 at 10(-8) mol/l was similar to that by control cells. Pretreatment with E2 at 10(-9) mol/l or more resulted in dose-dependent increase in spontaneous [3H] DA release from the cultured hypothalamic cells. The spontaneous [3H] DA release reached almost a plateau on pretreatment with E2 at 10(-9) mol/l for 6 hours. Pretreatment with 1 nM E2 also enhanced DA release induced by 10 microM ionophore A23187. These results indicate that estrogen stimulates tuberoinfundibular DA neuronal activity.

摘要

利用来自大鼠下丘脑结节漏斗区的原代培养细胞（其中包括多巴胺能神经元），研究了17-β雌二醇（E2）对自发性[3H]多巴胺（[3H]DA）释放的影响。在10^(-8) mol/l的E2存在下，神经元对[3H]DA的摄取与对照细胞相似。用10^(-9) mol/l或更高浓度的E2预处理导致培养的下丘脑细胞自发性[3H]DA释放呈剂量依赖性增加。在用10^(-9) mol/l的E2预处理6小时后，自发性[3H]DA释放几乎达到平台期。用1 nM的E2预处理也增强了由10 microM离子载体A23187诱导的DA释放。这些结果表明雌激素刺激结节漏斗多巴胺能神经元的活性。