Makino Shinya, Hashimoto Kozo, Gold Philip W
Second Department of Internal Medicine, Kochi Medical School, Okoh-cho, Nankoku, Japan.
Pharmacol Biochem Behav. 2002 Aug;73(1):147-58. doi: 10.1016/s0091-3057(02)00791-8.
Stress-associated disorders such as melancholic depression are characterized by persistent hypothalamic-pituitary-adrenocortical (HPA) axis activation and intensive anxiety. Corticotropin-releasing hormone (CRH) appears to play an essential role in pathophysiology of such disorders. In an attempt to elucidate possible mechanisms underlying persistent activation of CRH in the central nervous system (CNS), we examined responses of hypothalamic and extrahypothalamic CRH systems to the stressors (immobilization stress or psychological stress) and interactions between these CRH systems and glucocorticoids in rats. We propose multiple feedback loops activating central CRH system: (1) attenuation of glucocorticoid-induced negative feedback on the activity of the hypothalamic and brainstem nuclei during chronic stress, (2) autoregulation of CRH biosynthesis in the hypothalamic paraventricular nucleus (PVN) through up-regulation of Type-1 CRH receptor (CRHR-1), and (3) glucocorticoid-mediated positive effects on the amygdaloid CRH system. Stress initially activates the hypothalamic CRH system, resulting in the hypersecretion of glucocorticoids from the adrenal gland. In addition, the psychological component of the stressor stimulates the amygdaloid CRH system. In the chronic phase of stress, down-regulation of GR in the PVN and other brain structures such as the locus coeruleus (LC) fails to restrain hyperfunction of the HPA axis, and persistent activation of the HPA axis further up-regulates the amygdaloid CRH system. Thus, the hypothalamic and the amygdaloid CRH systems cooperatively constitute stress-responsive, anxiety-producing neurocircuitry during chronic stress, which is responsible for the clinical manifestations of stress-associated disorders. Effects of tricyclic antidepressants (TCAs), which appear to mitigate the above mentioned multiple feedback loop forming the vicious circle to activate central CRH systems, will also be discussed.
诸如忧郁症等与应激相关的疾病,其特征在于下丘脑 - 垂体 - 肾上腺皮质(HPA)轴持续激活以及强烈焦虑。促肾上腺皮质激素释放激素(CRH)似乎在此类疾病的病理生理学中起关键作用。为了阐明中枢神经系统(CNS)中CRH持续激活的潜在机制,我们研究了下丘脑和下丘脑外CRH系统对应激源(束缚应激或心理应激)的反应,以及这些CRH系统与大鼠体内糖皮质激素之间的相互作用。我们提出了多个激活中枢CRH系统的反馈回路:(1)慢性应激期间糖皮质激素对下丘脑和脑干核团活动的负反馈减弱;(2)通过上调1型CRH受体(CRHR - 1)对下丘脑室旁核(PVN)中CRH生物合成进行自动调节;(3)糖皮质激素对杏仁核CRH系统的正性作用。应激最初激活下丘脑CRH系统,导致肾上腺糖皮质激素分泌过多。此外,应激源的心理成分刺激杏仁核CRH系统。在应激的慢性阶段,PVN以及其他脑结构如蓝斑(LC)中糖皮质激素受体(GR)的下调无法抑制HPA轴的功能亢进,而HPA轴的持续激活进一步上调杏仁核CRH系统。因此,下丘脑和杏仁核CRH系统在慢性应激期间协同构成应激反应性、产生焦虑的神经回路,这与应激相关疾病的临床表现有关。还将讨论三环类抗抑郁药(TCA)的作用,其似乎减轻了上述形成恶性循环以激活中枢CRH系统的多个反馈回路。