Van Loon G R, Shum A, Ho D
Peptides. 1982 Sep-Oct;3(5):799-803. doi: 10.1016/0196-9781(82)90018-3.
Catecholamine and serotonin neurons in the hypothalamus regulate the secretion of corticotropin releasing factor (CRF). We considered the possibility that CRF might in turn affect the activity of these aminergic neurons. We examined the effect of intracisternal administration of synthetic CRF on the synthesis turnover rates of dopamine and serotonin in the hypothalamus of adult male rats using two different methods to assess turnover. In one study, we measured the accumulation of L-dihydroxyphenylalanine (L-DOPA) or 5-hydroxytryptophan (5-HTP) in mediobasal hypothalamus after L-aromatic amino acid decarboxylase inhibition with m-hydroxybenzylhydrazine 20 min before sacrifice, and in the second study we measured the accumulation of dopamine, norepinephrine, epinephrine and serotonin after monoamine oxidase inhibition with pargyline 20 min before sacrifice. The commercial CRF which we administered intraarterially increased plasma ACTH and corticosterone concentrations. Intracerebral CRF 5 to 20 micrograms 20 min before sacrifice or 20 micrograms 110 min before sacrifice did not alter the m-hydroxybenzylhydrazine-induced accumulation of L-DOPA or 5-HTP when compared with saline vehicle-injected controls. CRF 20 micrograms did not alter basal concentration or pargyline-induced accumulation of the catecholamines or serotonin in whole hypothalamus when compared with saline vehicle-injected controls. Thus, intracisternal administration of CRF did not alter hypothalamic dopamine or serotonin synthesis rates as assessed by two nonsteady state turnover methods. The data suggest that the release of CRF from neurons in hypothalamus does not alter the activity of catecholamine or serotonin neurons in the hypothalamus of normal adult male rats.
下丘脑的儿茶酚胺能和5-羟色胺能神经元调节促肾上腺皮质激素释放因子(CRF)的分泌。我们考虑了CRF可能反过来影响这些胺能神经元活性的可能性。我们使用两种不同的方法评估更新率,研究了成年雄性大鼠脑池内注射合成CRF对下丘脑多巴胺和5-羟色胺合成更新率的影响。在一项研究中,我们在处死前20分钟用间羟基苄基肼抑制L-芳香族氨基酸脱羧酶后,测量了下丘脑内侧基底部L-二羟基苯丙氨酸(L-DOPA)或5-羟色氨酸(5-HTP)的蓄积,在第二项研究中,我们在处死前20分钟用优降宁抑制单胺氧化酶后,测量了多巴胺、去甲肾上腺素、肾上腺素和5-羟色胺的蓄积。我们动脉内注射的市售CRF增加了血浆促肾上腺皮质激素(ACTH)和皮质酮的浓度。与注射生理盐水的对照组相比,处死前20分钟脑室内注射5至20微克CRF或处死前110分钟注射20微克CRF,并没有改变间羟基苄基肼诱导的L-DOPA或5-HTP的蓄积。与注射生理盐水的对照组相比,20微克CRF并没有改变整个下丘脑儿茶酚胺或5-羟色胺的基础浓度或优降宁诱导的蓄积。因此,通过两种非稳态更新方法评估,脑池内注射CRF并没有改变下丘脑多巴胺或5-羟色胺的合成率。数据表明,下丘脑神经元释放的CRF并不会改变正常成年雄性大鼠下丘脑儿茶酚胺能或5-羟色胺能神经元的活性。