TUBEROINFUNDIBULAR DOPAMINE NEURONS AND PROLACTIN

本研究旨在进一步阐明漏斗结节的作用。 多巴胺能(TIDA)神经元在催乳素(PRL)和 大鼠垂体前叶的促黄体生成素(LH)。 灵敏的神经化学分析与显微解剖方法相结合 测定脑组织中神经递质和促黄体生成素释放激素功能的变化 大鼠离散核、纤维通路和终末投射野 大脑。内侧(Mem)和内侧(Mem)TIDA终末的神经元活动 横向(MEL)正中隆起将相互对比，并与 在受控期间其他已知的多巴胺和去甲肾上腺素能投射 催乳素和促黄体生成素分泌的内分泌调控。特定于TIDA的更改 因此，神经元可以被识别并与PRL和LH滴度相关联。 外周循环。神经元的活动将由五个人评估 指标：(1)多巴胺和去甲肾上腺素的测定 周转率，(2)儿茶酚胺代谢产物的测定，(3)测定 门静脉血中DA和LH-RH的含量；(4)~3H-2-脱氧葡萄糖放射自显影； 以及(5)使用正中隆起突触小体准备来研究 调节多巴胺和黄体生成素释放的化合物。试析《中国日报》 哺乳诱导的催乳素升高将需要估计 在这个戏剧性的过程中，Mem和Mel中的TIDA神经元活动 神经内分泌反应。一种定量和时程研究的方法 催乳素对TIDA神经元的短环负反馈作用 已执行。TIDA神经元在β-内啡肽引起的兴奋中的作用 和2-溴-α-麦角隐亭(CB-154)诱导的PRL分泌减少 将会被研究。高催乳素血症对下丘脑的影响 涉及黄体生成素释放的机制将在完整的、去势的和 类固醇取代了雄性和雌性大鼠，在哺乳期大鼠和自行车运动中 老鼠。这些免费的模型提供了受控的内分泌环境 以检查内源性PRL高分泌的影响，或者 外源性给予PRL，对促黄体生成素释放机制的影响。这些 研究基于两个工作假设：(1)TIDA神经元的功能是 催乳素抑制因子(PIF)神经分泌神经元和(2)仅 投射到MEM的TIDA神经元起PIF神经元的作用，而投射到MEM的TIDA神经元 终止于MEL的是抑制促黄体生成素释放的神经调节剂。

This research seeks to further elucidate the role of tuberoinfundibular dopaminergic (TIDA) neurons in the release of prolactin (PRL) and luteinizing hormone (LH) from the anterior pituitary gland in the rat. Sensitive neurochemical assays combined with a microdissection method allow for the measurement of changes in neurotransmitter and LH-RH function in discrete nuclei, fiber pathways and terminal projection fields of the rat brain. The neuronal activity of TIDA terminals in the medial (MEm) and lateral (MEl) median eminence will be contrasted with each other and with other known dopaminergic and noradrenergic projections during controlled endocrine manipulations of PRL and LH secretion. Changes specific to TIDA neurons may thus be identified and correlated with PRL and LH titers in the peripheral circulation. Neuronal activity will be assessed by five indices: (1) the determination of dopamine (DA) and norepinephrine (NE) turnover, (2) measurement of catecholamine metabolites, (3) determination of DA and LH-RH in portal blood, (4) 3H-2-deoxy-glucose autoradiography, and (5) the use of median eminence synaptosome preparations to study compounds which modulate DA and LH-RH release. An analysis of the suckling-induced rise in PRL will be undertaken entailing estimation of TIDA neuronal activity in the MEm and MEl during this dramatic neuroendocrine response. A quantitative and time course study of the short-loop negative feedback action of PRL on TIDA neurons will be performed. The role of TIDA neurons in the Beta-endorphin-induced increase and 2-brom-Alpha-ergocriptine (CB-154)-induced decrease in PRL secretion will be studied. The effects of hyperprolactinemia on hypothalamic mechanisms involved in LH release will be studied in intact, castrated and steroid replaced male and female rats, in lactating rats and in the cycling rat. These complimentary models provide controlled endocrine environments in which to examine the effect of either endogenous PRL hypersecretion, or exogenously administered PRL, on the LH-RH release mechanism. These studies bear on two working hypotheses: (1) that TIDA neurons function as prolactin inhibitory factor (PIF) neurosecretory neurons and (2) that only the TIDA neurons projecting to the MEm function as PIF neurons while those terminating in the MEl are inhibitory neuromodulators of LH-RH release.