Different control of the adrenocorticotropin-corticosterone response and of prolactin secretion during cold stress, anesthesia, surgery, and nicotine injection in the rat: involvement of capsaicin-sensitive sensory neurons.
Different control of the adrenocorticotropin-corticosterone response and of prolactin secretion during cold stress, anesthesia, surgery, and nicotine injection in the rat: involvement of capsaicin-sensitive sensory neurons.
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大鼠冷应激、麻醉、手术和尼古丁注射期间促肾上腺皮质激素-皮质酮反应和催乳素分泌的不同控制：辣椒素敏感感觉神经元的参与。
DOI：
10.1210/endo-126-2-921
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发表时间：
1990
期刊：
影响因子：
4.8
通讯作者：
F. Lembeck
中科院分区：
文献类型：
--
作者：
J. Donnerer;F. Lembeck
比较了缺乏传入C纤维的辣椒素处理大鼠和对照组在躯体感觉(冷、手术)和中枢(束缚)应激状态下ACTH、皮质酮和催乳素的释放。冷应激诱导ACTH的释放，从而导致皮质酮的释放，但在辣椒素处理的大鼠中不能。静脉注射ACTH1-24对两组释放皮质酮的效果相同。冷应激不释放PRL，束缚应激能诱导ACTH和PRL的释放，辣椒素处理组和对照组均如此。戊巴比妥钠麻醉可引起PRL，但不能释放ACTH。在戊巴比妥钠麻醉下手术可引起ACTH释放，但可被辣椒素预先阻断。手术后PRL水平不再进一步升高。根据降压反射的观察，小剂量尼古丁(动脉内注射5微克)可刺激传入C纤维。腹腔注射尼古丁(250微克/公斤)可引起辣椒素处理的清醒大鼠和对照大鼠血浆ACTH的显著升高，这可能是由于中枢刺激所致，因为这种作用在戊巴比妥麻醉期间被抑制。清醒大鼠可见尼古丁引起的催乳素水平适度升高。所使用的刺激被视为应激的实验模型，它们在激发ACTH、皮质酮和催乳素释放的能力方面显示出本质上的差异。那些通过传入C纤维刺激导致ACTH和皮质酮释放的刺激不会释放PRL，而情绪和认知应激导致ACTH和PRL的释放。
The release of ACTH, corticosterone, and PRL was compared in capsaicin-pretreated rats, which lack afferent C-fibers, and their controls under somatosensory (cold, surgery) and central (restraint) forms of stress. Cold stress induced the release of ACTH and consequently that of corticosterone in the controls, but not in the capsaicin-pretreated rats. Intravenous injection of ACTH1-24 was equally effective in releasing corticosterone in both groups. Whereas PRL was not released in response to cold stress, restraint stress did induce the release of both ACTH and PRL, in the capsaicin-pretreated as well as in the control group. Pentobarbital anesthesia alone elicited PRL, but no ACTH release. ACTH release was evoked by surgery under pentobarbital anesthesia but was abolished by capsaicin pretreatment. PRL levels were not further increased by surgery. Nicotine in a small dose (5 micrograms intra-arterially) evoked stimulation of afferent C-fibers as observed on a depressor reflex. Intraperitoneal injection of nicotine (250 micrograms/kg) caused a marked rise in plasma ACTH both in the capsaicin-pretreated conscious rats and in their controls, probably resulting from central stimulation as this effect was shown to be inhibited during pentobarbital anesthesia. A moderate rise of PRL by nicotine was seen in conscious rats. The stimuli used, regarded as experimental models of stress, show essential differences in their ability to evoke the release of ACTH, corticosterone, and PRL. Those stimuli which cause the release of ACTH and corticosterone via afferent C-fiber stimulation do not release PRL, whereas emotional and cognitive stress causes the release of both ACTH and PRL.