ESTROGEN MODULATION OF THE ALPHA-1-ADRENERGIC RESPONSE OF HYPOTHALAMIC NEURONS
ESTROGEN MODULATION OF THE ALPHA-1-ADRENERGIC RESPONSE OF HYPOTHALAMIC NEURONS
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DOI：
10.1159/000125201
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发表时间：
1989-07-01
影响因子：
4.1
通讯作者：
KELLY, MJ
中科院分区：
文献类型：
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作者：
CONDON, TP;RONNEKLEIV, OK;KELLY, MJ
对完整、卵巢切除和卵巢切除加雌二醇-苯甲酸酯处理的雌性豚鼠矢状面切片的106个弓形和细胞贫区（ARC-CPZ）神经元进行细胞内记录，并观察去甲肾上腺素（NE）、。1-激动剂甲氧沙明（MX）和。检测激动剂异丙肾上腺素。适用于2-100亩的水浴或压力施用。mne可逆超极化并抑制大多数（57%,n = 60） ARC-CPZ神经元的自发放电。异丙肾上腺素对大部分（75%）ARC-CPZ神经元也有抑制作用。此外，还有2-100亩。M - NE使20% （n = 21）的ARC-CPZ神经元去极化和/或自发活动增加，其中部分（n = 8）神经元表现出爆裂活动。相同剂量的MX在48% （n = 14）的ARC-CPZ神经元中模拟了NE兴奋（去极化和/或增加放电）。根据血清中17 - β的水平。-雌二醇，将三组雌性分为高雌激素组（bbb30 pg/ml）和低雌激素组（< 30 pg/ml），发现内源性或外源性雌激素显著增加了MX反应神经元的数量（从29%增加到75%）。使用细胞内标记与proproon黄色和免疫细胞化学，我们已经确定黄体生成素释放激素神经元响应NE。因此，在哺乳动物促黄体激素排卵前激增时，去肾上腺素能兴奋驱动增加的一种机制是神经元对。α的反应增加。1-adrenergic刺激。
Intracellular recordings were made from 106 arcuate and cell-poor zone (ARC-CPZ) neurons in sagittal slices prepared from intact, ovariectomized and ovariectomized plus estradiol-benzoate-treated female guinea pigs, and the effect of norepinephrine (NE), the .alpha.1-agonist methoxamine (MX) and the .beta.-agonist isoproterenol were tested. Either bath application or pressure application of 2-100 .mu.M NE reversibly hyperpolarized and inhibited the spontaneous firing of the majority (57%, n = 60) of ARC-CPZ neurons. Isoproterenol also inhibited the majority (75%) of the ARC-CPZ neurons which it was tested on. In addition, 2-100 .mu.M NE depolarized and/or increased the spontaneous activity of 20% (n = 21) of ARC-CPZ neurons, and some of these (n = 8) exhibited bursting activity. Similar doses of MX mimicked the NE excitation (depolarization and/or increasing firing) in 48% (n = 14) of the ARC-CPZ neurons tested. Based on the serum levels of 17.beta.-estradiol, the three groups of females were divided into high (> 30 pg/ml) and low (< 30 pg/ml) estrogen groups, and it was found that endogenous or exogenous estrogen significantly increased the number of neurons responding to MX (from 29 to 75%). USing intracellular labeling with procion yellow and immunocytochemistry, we have identified that luteinizing hormone-releasing hormone neurons respond to NE. Therefore, it is suggested that one mechanism for an increase in the noradrenergic excitatory drive at the time of the preovulatory surge of luteinizing hormone in the mammal is an increase in the neuronal response to .alpha.1-adrenergic stimulation.