ELECTROPHYSIOLOGICAL EVIDENCE FOR FACILITATORY CONTROL OF OXYTOCIN NEURONS BY OXYTOCIN DURING SUCKLING IN THE RAT
ELECTROPHYSIOLOGICAL EVIDENCE FOR FACILITATORY CONTROL OF OXYTOCIN NEURONS BY OXYTOCIN DURING SUCKLING IN THE RAT
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DOI：
10.1113/jphysiol.1984.sp015302
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发表时间：
1984-01-01
影响因子：
5.5
通讯作者：
RICHARD, P
中科院分区：
文献类型：
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作者：
FREUNDMERCIER, MJ;RICHARD, P
在乌拉坦(1.2g/kg)麻醉大鼠哺乳过程中，与乳房内压同步记录室旁神经元。这些神经元的放电模式与排乳相关，这使得催产素和加压素神经元得以区分。催产素神经元表现出一种短的(2-6个S)特征的高频棘波爆发。这种激活可能同时发生在所有催产素神经元12-18 S排乳前，并且在频率和幅度(峰总数)上都是有规律的。研究了神经垂体肽及其类似物在控制这些特性中的作用。第三脑室注射催产素10pg、100pg和1 ng可增加慢放电催产素神经元的背景活动(~lt；3个峰/S)，并对乳汁喷射反射有强烈的易化作用，增加神经分泌爆发的幅度和频率。未观察到对非神经分泌神经元的影响。这样的注射也会在哺乳开始一小时后还没有出现的情况下触发排乳反射。催产素本身并不诱导神经分泌激活，只有在幼鼠哺乳时才会出现这种激活。侧脑室注射催产素的效果不如第三脑室。静脉血或第四脑室注射后未见作用，提示催产素作用于下丘脑。向第三脑室注射中胚素或异催产素具有与催产素相似的易化作用，但加压素、加压素、MIF I(ProLeu-Gly-NH2，末端三联体催产素)或牛神经生理素I和II不改变神经分泌激活或乳汁排出模式。向第三脑室注射催产素拮抗剂([1(β-巯基-β，β-环戊亚甲基-丙酸)，8-鸟氨酸]血管催产素，d(CH2)5OVT)可降低排乳频率，显著延迟第一次排乳。这是因为神经分泌爆发的频率和幅度都降低了，以至于不能引起可检测到的催产素释放；d(CH2)5OVT抑制了外源性催产素的易化作用。在正常情况下，内源性催产素似乎参与了神经分泌激活的控制。
Antidromically identified paraventricular neurons were recorded simultaneously with intramammary pressure in urethane (1.2 g/kg) anesthetized rats during suckling. The correlation of the firing pattern of these neurons with milk ejection enabled distinction between oxytocin and vasopressin neurons. Oxytocin neurons displayed a short (2-6 s) characteristic high-frequency burst of spikes. This activation probably occurred simultaneously in all oxytocin neurons 12-18 s before milk ejection and was regular in both frequency and amplitude (total number of spikes). The role of neurohypophyseal peptides and analogs in the control of these characteristics was studied. Injecting 10 pg, 100 pg and 1 ng of oxytocin into the 3rd ventricle increased background activity of slow-firing oxytocin neurons (< 3 spikes/s) and had a strong dose-dependent facilitatory effect on the milk ejection reflex, increasing both the amplitude and frequency of neurosecretory bursts. No effect was observed on non-neurosecretory neurons. Such injection also triggered the milk ejection reflex when it had not appeared an hour after suckling began. Oxytocin did not itself induce neurosecretory activation, which only appeared if the young rats were suckling. Injecting oxytocin into the lateral ventricle was less effective than into the 3rd ventricle. No effect was observed after injection into the venous blood or into the 4th ventricle, which suggested that oxytocin acts in the hypothalamus. Injection of mesotocin or isotocin into the 3rd ventricle had a facilitatory effect similar to that of oxytocin but vasopressin, vasotocin, MIF I (pro-leu-gly-NH2, terminal triplet oxytocin) or bovine neurophysins I and II did not modify neurosecretory activation or the milk ejection pattern. Injecting an oxytocin antagonist, ([1(.beta.-mercapto-.beta.,.beta.-cyclopentamethylene-propionic acid), 8-ornithine]vasotocin, d(CH2)5OVT) into the 3rd ventricle decreased milk ejection frequency and considerably delayed the reappearance of the 1st milk ejection. This resulted from a decrease in both frequency and amplitude of neurosecretory bursts, which were too small to induce detectable oxytocin release; d(CH2)5OVT suppressed the facilitatory effect of exogenous oxytocin. Under normal conditions, endogenous oxytocin seemed to be involved in the control of neurosecretory activation.