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雌性大鼠中,结节漏斗多巴胺能神经元对催乳素的反应性随年龄增长而丧失。

Age-related loss of the responsiveness of the tuberoinfundibular dopaminergic neurons to prolactin in the female rat.

作者信息

Reymond M J

机构信息

Department of Internal Medicine, University Hospital, Lausanne, Switzerland.

出版信息

Neuroendocrinology. 1990 Nov;52(5):490-6. doi: 10.1159/000125633.

Abstract

In the old female rat the previous findings of a sustained reduction of the secretory activity of the hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons associated with a persistent hyperprolactinemia as well as the observation of a failure of the prolactin (PRL) short-loop feedback mechanism have been suggestive of an age-related loss of the responsiveness of the TIDA neurons to the stimulatory action of PRL. Yet the existence of significant impairments in the capacity of the neurons to respond to PRL could not be demonstrated in an earlier study using multiparous old rats in constant estrus compared to young nulliparous estrous rats. In the present study we have readdressed the issue using nulliparous old rats (24-26 months) compared to virgin young rats (4-5 months); two sets of old rats were studied which displayed distinct senile reproductive states, namely persistent diestrus or repetitive pseudopregnancy, and they were compared to young rats in diestrus or in repetitive pseudopregnancy, respectively. The secretory activity of the TIDA neurons was evaluated by measurement of dopamine biosynthesis in the neurons (DOPA accumulation in the median eminence after decarboxylase inhibition) and dopamine release into hypophysial portal blood, and PRL influence on the activity of the TIDA neurons was studied after repeated s.c. administrations of ovine PRL (oPRL) or the solvent vehicle. A reduced activity of the TIDA neurons was observed in both groups of nulliparous aged rats compared to their respective young control group.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在老年雌性大鼠中,先前的研究结果表明,下丘脑结节漏斗多巴胺能(TIDA)神经元的分泌活动持续降低,伴有持续性高催乳素血症,同时观察到催乳素(PRL)短环反馈机制失效,这提示TIDA神经元对PRL刺激作用的反应性存在与年龄相关的丧失。然而,在一项早期研究中,与年轻未生育的发情期大鼠相比,使用处于持续发情期的经产老年大鼠,未能证明神经元对PRL反应能力存在显著损害。在本研究中,我们使用未生育的老年大鼠(24 - 26个月)与年轻的处女大鼠(4 - 5个月)重新探讨了这个问题;研究了两组处于不同老年生殖状态的老年大鼠,即持续动情间期或重复性假孕,并分别将它们与处于动情间期或重复性假孕的年轻大鼠进行比较。通过测量神经元中的多巴胺生物合成(脱羧酶抑制后正中隆起处的多巴积累)以及多巴胺释放到垂体门脉血中的情况来评估TIDA神经元的分泌活动,并在多次皮下注射羊催乳素(oPRL)或溶剂载体后研究PRL对TIDA神经元活动的影响。与各自的年轻对照组相比,两组未生育的老年大鼠均观察到TIDA神经元活性降低。(摘要截断于250字)

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