CHANGES IN LUTEINIZING-HORMONE AND PROLACTIN CONTROL MECHANISMS PRODUCED BY GLUTAMATE LESIONS OF ARCUATE NUCLEUS
CHANGES IN LUTEINIZING-HORMONE AND PROLACTIN CONTROL MECHANISMS PRODUCED BY GLUTAMATE LESIONS OF ARCUATE NUCLEUS
复制标题
DOI：
10.1210/endo-103-4-1304
复制
发表时间：
1978-01-01
期刊：
影响因子：
4.8
通讯作者：
SHAAR, CJ
中科院分区：
文献类型：
--
作者：
CLEMENS, JA;ROUSH, ME;SHAAR, CJ
在大鼠出生后第2、4、6、10天，以4 g/kg谷氨酸钠灌胃，形成弓形核和视网膜病变，3 ~ 5月龄时继续实验。在新生期接受谷氨酸治疗的成年大鼠中，弓形核中细胞体的数量显著减少，视觉系统明显退化，垂体前叶、卵巢、子宫、睾丸和精囊变小。在谷氨酸处理组中，多巴胺浓度降低了60%，并且出现了不规则的发情周期。在6组谷氨酸处理的大鼠中，有2组的基础血清LH水平低于对照组，而在6组中有1组的催乳素水平升高。其余谷氨酸处理组的基础血清PRL或LH水平无显著变化。卵巢切除后，谷氨酸处理的大鼠血清LH水平低于对照组，谷氨酸处理大大减弱了苯甲酸雌二醇治疗后卵巢切除大鼠血清LH和PRL的激增。虽然谷氨酸处理明显减少了雌激素治疗的去卵巢大鼠PRL的释放，但5-羟色氨酸（5-HTP）治疗后则相反。在雄性和雌性大鼠中，谷氨酸处理组在30 mg/kg 5-HTP的作用下，PRL的释放明显增强。谷氨酸大鼠5-HTP处理后PRL的释放量显著大于阻断多巴胺受体后PRL的释放量。当雌激素为诱导剂时，谷氨酸诱导的弓形核病变可能导致LH和PRL的释放机制受损，但会产生血清素能刺激在释放PRL方面更有效的情况。血清素可能通过PRL释放因子释放PRL。
Lesions of the arcuate nucleus and retina were produced by i.p. administration of 4 g/kg monosodium glutamate to rats on days 2, 4, 6 and 10 after birth, and all experimental work was continued at about 3-5 mo. of age. A striking reduction in the number of cell bodies in the arcuate nucleus, a marked degeneration of the visual system, and smaller anterior pituitaries, ovaries, uteri, testes and seminal vesicles were noted in adult rats that had been treated with glutamate during the neonatal period. A 60% reduction in the concentration of dopamine in the medial-basal hypothalamus and irregular estrous cycles also were observed in glutamate-treated groups. In 2 of 6 groups of glutamate-treated rats, basal serum LH [luteinizing hormone] levels were lower than in controls, whereas in 1 of 6 groups, PRL [prolactin] was elevated. The remainder of glutamate-treated groups showed no significant change in basal serum PRL or LH levels. After ovariectomy, serum LH levels were lower in glutamate-treated rats than in controls, and glutamate treatment greatly attenuated the surges of LH and PRL seen in ovariectomized rats after treatment with estradiol benzoate. Although glutamate treatment markedly attenuated the release of PRL in ovariectomized rats treated with estrogen, the opposite was true after 5-hydroxytryptophan (5-HTP). In both male and female rats, a marked enhancement of PRL release in response to 30 mg/kg 5-HTP was observed in glutamate-treated groups. The release of PRL after 5-HTP treatment in glutamate rats was significantly greater than the release of PRL after blockade of dopamine receptors. Glutamate-induced lesions of the arcuate nucleus may result in an impaired release mechanism for LH and PRL when estrogen is the inducer, but produce a condition where serotonergic stimuli are much more effective in releasing PRL. Serotonin may release PRL through a PRL-releasing factor.