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阿片类药物与麻醉的妊娠大鼠第三脑室前周输入与催产素神经元的耦合

Opioids and coupling of the anterior peri-third ventricular input to oxytocin neurones in anaesthetized pregnant rats.

作者信息

Bull P M, Douglas A J, Russell J A

机构信息

Department of Physiology, Edinburgh University Medical School, Scotland, UK.

出版信息

J Neuroendocrinol. 1994 Jun;6(3):267-74. doi: 10.1111/j.1365-2826.1994.tb00582.x.

DOI:10.1111/j.1365-2826.1994.tb00582.x
PMID:7920592
Abstract

In the pregnant rat the osmotic drive to oxytocin neurones is reduced and oxytocin secretion itself is inhibited by endogenous opioids. Coupling of the anterior peri-third ventricular input pathway, involved in osmoregulation, to magnocellular oxytocin neurones was studied in urethane-anaesthetized virgin and 21 day pregnant rats using electrical stimulation of the region anterior and ventral to the third cerebral ventricle (AV3V region) to drive the oxytocin neurones, and giving naloxone to prevent the action of any endogenous opioids on the system. Trains of stimuli (0.5 mA, 1 ms pulses, 10 s on 10 s off, at either 10 Hz or 25 Hz for 10 or 2 min respectively) were given at 20 or 30 min intervals via an electrode stereotaxically-implanted in the AV3V region, and femoral arterial blood plasma samples collected immediately before and after each stimulation were radioimmunoassayed for oxytocin concentration. The first (control) AV3V stimulation increased plasma oxytocin concentration reproducibly and similarly in virgin and 21-day pregnant rats. Naloxone administered 10 min before the second stimulus increased basal plasma oxytocin concentration in virgin and pregnant rats and increased the oxytocin secretory response to 25 Hz AV3V stimulation in virgin but not pregnant rats, and the response was significantly greater in virgin rats. Naloxone reveals oxytocin secretion unrestrained by endogenous opioids, therefore it appears that there is an opioid-independent reduction in the excitatory coupling of the AV3V input to oxytocin neurones which may explain the reduced osmoresponsiveness of oxytocin neurones at the end of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在妊娠大鼠中,催产素神经元的渗透驱动力降低,内源性阿片类物质抑制催产素的分泌本身。在氨基甲酸乙酯麻醉的未孕和妊娠21天的大鼠中,研究了参与渗透压调节的第三脑室前周围输入通路与大细胞催产素神经元的耦合情况。通过电刺激第三脑室前腹侧区域(AV3V区域)来驱动催产素神经元,并给予纳洛酮以防止任何内源性阿片类物质对该系统的作用。通过立体定向植入AV3V区域的电极,每隔20或30分钟给予一系列刺激(0.5 mA,1 ms脉冲,10秒开10秒关,分别以10 Hz或25 Hz持续10或2分钟),并对每次刺激前后立即采集的股动脉血浆样本进行放射免疫测定催产素浓度。首次(对照)AV3V刺激在未孕和妊娠21天的大鼠中可重复且相似地增加血浆催产素浓度。在第二次刺激前10分钟给予纳洛酮,可增加未孕和妊娠大鼠的基础血浆催产素浓度,并增加未孕大鼠对25 Hz AV3V刺激的催产素分泌反应,但对妊娠大鼠无此作用,且未孕大鼠的反应明显更大。纳洛酮揭示了内源性阿片类物质未抑制的催产素分泌,因此似乎存在AV3V输入与催产素神经元兴奋性耦合的阿片类物质非依赖性降低,这可能解释了妊娠末期催产素神经元渗透压反应性降低的原因。(摘要截短至250字)

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