NEUROENDOCRINE REGULATION OF PROLACTIN SECRETION

本研究旨在进一步阐明漏斗结节的作用。 多巴胺能(TIDA)神经元参与催乳素(PRL)的释放 大鼠的脑垂体腺。介绍了一种显微解剖技术。 它允许离散地移除原子核、终端投影场和 来自大鼠大脑的纤维通路。高灵敏材料的发展 多巴胺(DA)、去甲肾上腺素(NE)和 3，4-二羟基苯乙酸(DOPAC)现在可以测定DA和 显微解剖脑内NE周转和主要DA代谢物DOPAC 地区。总之，这些微技术使神经化学分析成为可能 神经内分泌事件的分辨率比以前高得多 有可能。神经元活性将通过两个神经化学指数进行评估：(1) 多巴胺和去甲肾上腺素周转率的测定(α-甲基对酪氨酸法)，以及 (2)DOPAC组织浓度测定。神经化学动力学研究进展 正中隆起(ME)的TIDA终末将与其他已知的 多巴胺能投射至尾状核、嗅结节和内侧 PRL分泌的受控内分泌操作中的视前核。 因此，TIDA神经元特有的变化可能被识别并与PRL相关 用直接放射免疫测定法测定外周循环中的滴度。 将对哺乳诱导的催乳素升高进行神经化学分析。 在这一戏剧性的过程中需要估计TIDA神经元的活动 神经内分泌反应。催乳素对TIDA的短环负反馈作用 将对去垂体大鼠的神经元进行研究。作用的神经部位 临床上用于抑制催乳素的药物2-溴-α-麦角隐亭(CB-154) 分泌物和治疗帕金森氏症的研究将在 TIDA神经元的水平。这些实验与工作假说有关 TIDA神经元作为催乳素抑制因子(PIF)的神经分泌功能 神经元。

This research seeks to further elucidate the role of tuberoinfundibular dopaminergic (TIDA) neurons in the release of prolactin (PRL) from the anterior pituitary gland in the rat. A microdissection technique has been introduced which allows for the discrete removal of nuclei, terminal projection fields and fiber pathways from the rat brain. The development of highly sensitive radioisotopic-enzymatic assays for dopamine (DA), norepinephrine (NE) and 3,4-dihydroxyphenylacetic acid (DOPAC) now allow for the determination of DA and NE turnover and the major DA metabolite DOPAC in such microdissected brain regions. In concert, these microtechniques allow for the neurochemical analysis of neuroendocrine events at a level of resolution far greater than previously possible. Neuronal activity will be assessed by two neurochemical indices: (1) the determination of DA and NE turnover (alpha-methyl-para-tyrosine method), and (2) measurement of DOPAC tissue concentrations. The neurochemical dynamics of TIDA terminals in the median eminence (ME) will be contrasted with other known dopaminergic projections to the caudate nucleus, olfactory tubercle and medial preoptic nucleus during controlled endocrine manipulations of PRL secretion. Changes specific to TIDA neurons may thus be identified and correlated with PRL titers in the peripheral circulation as determined by direct radioimmunoassay. A neurochemical analysis of the suckling-induced rise in PRL will be undertaken entailing estimation of TIDA neuronal activity during this dramatic neuroendocrine response. The short-loop negative feedback action of PRL on TIDA neurons will be investigated in hypophysectomized rats. A neural site of action of 2-brom-alpha-ergocryptine (CB-154), a drug used clinically to inhibit PRL secretion and in the treatment of Parkinson's disease, will be investigated at the level of the TIDA neurons. These experiments bear on the working hypothesis that TIDA neurons function as prolacting inhibitory factor (PIF) neurosecretory neurons.