Gunnet J W, Moore K E
Department of Pharmacology and Toxicology, Michigan State University, East Lansing.
Neuroendocrinology. 1988 Jan;47(1):20-6. doi: 10.1159/000124885.
Perikarya and terminals of tuberoinfundibular dopaminergic (TIDA) neurons are located in the arcuate nucleus (ARN) and in the median eminence (ME), respectively. Dopamine (DA) released from TIDA terminals in the ME inhibits prolactin secretion from the anterior pituitary. Anatomical studies have described the sources of afferents to ARN and ME, but not to TIDA neurons per se. The ventromedial nucleus (VMN) and the dorsomedial nucleus (DMN) of the hypothalamus project to ARN and ME and have a role in prolactin regulation. In the present study, VMN and DMN were investigated as possible sources of TIDA afferents. Alterations in the activity of TIDA neurons were estimated by measuring plasma concentrations of prolactin and the rates of DA synthesis (3,4-dihydroxyphenylalanine - DOPA - accumulation after administration of the decarboxylase inhibitor NSD 1015) and metabolism (concentrations of the DA metabolite 3,4-dihydroxyphenylacetic acid - DOPAC) in the ME following electrical stimulation of ARN, VMN, and DMN in ovariectomized female rats. Thirty minutes of bilateral stimulation of ARN or DMN increased DOPA accumulation in the ME; stimulation of the VMN had no effect. 5-Hydroxytryptamine synthesis in the ME was unaffected by stimulation of any region. Plasma prolactin levels declined during DMN stimulation, varying with the frequency and duration of the electrical stimulus. DA metabolism within TIDA neurons increased with DMN stimulation, as evidenced by increased DOPAC concentrations in the ME. In females whose basal TIDA activity has been increased by haloperidol treatment or decreased by bromocriptine treatment, DMN stimulation was still able to increase DOPA accumulation in the ME. The present data suggest the presence of stimulatory TIDA afferents originating from or passing through the DMN.
结节漏斗多巴胺能（TIDA）神经元的胞体和终末分别位于弓状核（ARN）和正中隆起（ME）。从ME中TIDA终末释放的多巴胺（DA）抑制垂体前叶催乳素的分泌。解剖学研究已经描述了传入ARN和ME的神经纤维来源，但尚未涉及TIDA神经元本身的传入神经来源。下丘脑腹内侧核（VMN）和背内侧核（DMN）投射至ARN和ME，并在催乳素调节中发挥作用。在本研究中，对VMN和DMN作为TIDA传入神经可能来源进行了研究。通过测量催乳素的血浆浓度以及在去卵巢雌性大鼠中电刺激ARN、VMN和DMN后ME中DA合成速率（脱羧酶抑制剂NSD 1015给药后3,4-二羟基苯丙氨酸 - DOPA - 的蓄积）和代谢速率（DA代谢产物3,4-二羟基苯乙酸 - DOPAC的浓度），来评估TIDA神经元活性的变化。双侧刺激ARN或DMN 30分钟可增加ME中DOPA的蓄积；刺激VMN则无此作用。刺激任何区域均不影响ME中5-羟色胺的合成。在DMN刺激期间，血浆催乳素水平下降，且随电刺激的频率和持续时间而变化。DMN刺激使TIDA神经元内的DA代谢增加，ME中DOPAC浓度升高证明了这一点。在通过氟哌啶醇治疗使基础TIDA活性升高或通过溴隐亭治疗使其降低的雌性大鼠中，DMN刺激仍能够增加ME中DOPA的蓄积。目前的数据表明，存在起源于或经过DMN的刺激性TIDA传入神经。
