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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Footshock-induced changes in brain catecholamines and indoleamines are not mediated by CRF or ACTH.
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Footshock-induced changes in brain catecholamines and indoleamines are not mediated by CRF or ACTH.

机译：休克引起的脑儿茶酚胺和吲哚胺的变化不是由CRF或ACTH介导的。

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摘要

Stressful treatments have long been associated with increased activity of brain catecholaminergic and serotonergic neurons. An intracerebroventricular (icv) injection of the corticotropin-releasing factor (CRF) also activates brain catecholaminergic neurons. Because brain CRF-containing neurons appear to be activated during stress, it is possible that CRF mediates the catecholaminergic activation. This hypothesis has been tested by assessing the responses in brain catecholamines and indoleamines to footshock in mice pretreated icv with a CRF receptor antagonist, and in mice lacking the gene for CRF (CRFko mice). Consistent with earlier results, icv administration of CRF increased catabolites of dopamine and norepinephrine, but failed to alter tryptophan concentrations or serotonin catabolism. A brief period of footshock increased plasma corticosterone and the concentrations of tryptophan and the catabolites of dopamine, norepinephrine and serotonin in several brain regions. Mice injected icv with 25 microg alpha-helical CRF(9-41) prior to footshock had neurochemical responses that were indistinguishable from controls injected with vehicle, while the increase in plasma corticosterone was slightly attenuated in some experiments. CRFko mice exhibited neurochemical responses to footshock that were indistinguishable from wild-type mice. However, whereas wild-type mice showed the expected increase in plasma corticosterone, there was no such increase in CRFko mice. Similarly, hypophysectomized mice also showed normal neurochemical responses to footshock, but no increase in plasma corticosterone. Hypophysectomy itself elevated brain tryptophan and catecholamine and serotonin metabolism. Treatment with ACTH icv or peripherally failed to induce any changes in cerebral catecholamines and indoleamines. These results suggest that CRF and its receptors, and ACTH and other pituitary hormones, are not involved in the catecholamine and serotonin responses to a brief period of footshock.
机译：长期以来，压力治疗与脑儿茶酚胺能和血清素能神经元的活动增加有关。脑室内（ICV）注射促肾上腺皮质激素释放因子（CRF）也可激活脑儿茶酚胺能神经元。因为包含CRF的大脑神经元在压力下似乎被激活，所以CRF可能介导儿茶酚胺能激活。通过评估用CRF受体拮抗剂预处理icv的小鼠和缺乏CRF基因的小鼠（CRFko小鼠）的大脑儿茶酚胺和吲哚胺对足部休克的反应，检验了该假设。与早期结果一致，CRF的icv给药增加了多巴胺和去甲肾上腺素的分解代谢产物，但未能改变色氨酸浓度或血清素分解代谢。短暂的休克期增加了几个大脑区域的血浆皮质酮和色氨酸的浓度，以及多巴胺，去甲肾上腺素和5-羟色胺的分解代谢产物。休克前用icv注射25μgα-螺旋CRF（9-41）的小鼠的神经化学反应与注射媒介物的对照组没有区别，而血浆皮质酮的增加在某些实验中略有减弱。 CRFko小鼠表现出对触电的神经化学反应，与野生型小鼠没有区别。但是，尽管野生型小鼠显示血浆皮质酮的预期增加，但CRFko小鼠却没有这种增加。类似地，经切除术切除的小鼠也显示出对足部休克的正常神经化学反应，但血浆皮质酮没有增加。垂体切除术本身会升高脑中的色氨酸和儿茶酚胺以及5-羟色胺的代谢。用ACTH icv或外围治疗无法诱导脑儿茶酚胺和吲哚胺的任何变化。这些结果表明，CRF及其受体，ACTH和其他垂体激素均不参与儿茶酚胺和5-羟色胺对短暂休克的反应。

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