Freund-Mercier M J, Richard P
J Physiol. 1984 Jul;352:447-66. doi: 10.1113/jphysiol.1984.sp015302.
Antidromically identified paraventricular neurones were recorded simultaneously with intramammary pressure in urethane (1.2 g/kg) anaesthetized rats during suckling. The correlation of the firing pattern of these neurones with milk ejection enabled distinction between oxytocin and vasopressin neurones. Oxytocin neurones displayed a short (2-6 s) characteristic high-frequency burst of spikes. This activation probably occurred simultaneously in all oxytocin neurones 12-18 s before milk ejection and was regular in both frequency and amplitude (total number of spikes). The role of neurohypophysial peptides and analogues 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 neurones (less than 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 neurones. 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 sucking. 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. Injecting 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 first milk ejection. This resulted from a decrease in both frequency and amplitude of neurosecretory bursts, which were too small to induce detectable oxytocin release. Moreover, 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. Injecting 1 ng oxytocin or 1 or 10 ng vasopressin into the 3rd ventricle did not modify the firing pattern of vasopressin neurones whether activated by hyperosmotic stimulation (1 ml NaCl, 9% solution (w/v) I.P.) or not.(ABSTRACT TRUNCATED AT 400 WORDS)
在哺乳期间，对氨基甲酸乙酯（1.2克/千克）麻醉的大鼠，同时记录逆向鉴定的室旁神经元和乳腺内压力。这些神经元的放电模式与乳汁排出的相关性，使得能够区分催产素神经元和血管加压素神经元。催产素神经元表现出短暂（2 - 6秒）的特征性高频放电爆发。这种激活可能在所有催产素神经元中于乳汁排出前12 - 18秒同时发生，并且在频率和幅度（放电总数）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征中的作用。向第三脑室内注射10皮克、100皮克和1纳克的催产素，增加了慢放电催产素神经元（每秒放电少于3次）的背景活动，并且对乳汁排出反射有强烈的剂量依赖性促进作用，增加了神经分泌爆发的幅度和频率。对非神经分泌神经元没有观察到影响。当哺乳开始一小时后乳汁排出反射未出现时，这种注射也能引发该反射。催产素本身不会诱导神经分泌激活，只有在幼鼠吸吮时才会出现。向侧脑室内注射催产素比向第三脑室内注射效果差。向静脉血或第四脑室内注射后未观察到影响，这表明催产素在下丘脑起作用。向第三脑室内注射中催产素或异催产素具有与催产素类似的促进作用，但血管加压素、加压催产素、MIF I（脯 - 亮 - 甘 - 氨，催产素的末端三联体）或牛神经垂体素I和II不会改变神经分泌激活或乳汁排出模式。向第三脑室内注射催产素拮抗剂（[1（β - 巯基 - β，β - 环戊亚甲基丙酸），8 - 鸟氨酸]加压催产素，d（CH2）5OVT）会降低乳汁排出频率，并显著延迟首次乳汁排出的再次出现。这是由于神经分泌爆发的频率和幅度降低，其幅度太小以至于无法诱导可检测到的催产素释放。此外，d（CH2）5OVT抑制了外源性催产素的促进作用。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。向第三脑室内注射1纳克催产素或1或10纳克血管加压素，无论是否通过高渗刺激（腹腔注射1毫升9%（重量/体积）氯化钠溶液）激活，都不会改变血管加压素神经元的放电模式。
