Uchoa E T, Aguilera G, Herman J P, Fiedler J L, Deak T, de Sousa M B C
Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao, Preto, SP, Brazil.
J Neuroendocrinol. 2014 Sep;26(9):557-72. doi: 10.1111/jne.12157.
Normal hypothalamic-pituitary-adrenal (HPA) axis activity leading to the rhythmic and episodic release of adrenal glucocorticoids (GCs) is essential for body homeostasis and survival during stress. Acting through specific intracellular receptors in the brain and periphery, GCs regulate behaviour, as well as metabolic, cardiovascular, immune and neuroendocrine activities. By contrast to chronic elevated levels, circadian and acute stress-induced increases in GCs are necessary for hippocampal neuronal survival and memory acquisition and consolidation, as a result of the inhibition of apoptosis, the facilitation of glutamatergic neurotransmission and the formation of excitatory synapses, and the induction of immediate early genes and dendritic spine formation. In addition to metabolic actions leading to increased energy availability, GCs have profound effects on feeding behaviour, mainly via the modulation of orexigenic and anorixegenic neuropeptides. Evidence is also emerging that, in addition to the recognised immune suppressive actions of GCs by counteracting adrenergic pro-inflammatory actions, circadian elevations have priming effects in the immune system, potentiating acute defensive responses. In addition, negative-feedback by GCs involves multiple mechanisms leading to limited HPA axis activation and prevention of the deleterious effects of excessive GC production. Adequate GC secretion to meet body demands is tightly regulated by a complex neural circuitry controlling hypothalamic corticotrophin-releasing hormone (CRH) and vasopressin secretion, which are the main regulators of pituitary adrenocorticotrophic hormone (ACTH). Rapid feedback mechanisms, likely involving nongenomic actions of GCs, mediate the immediate inhibition of hypothalamic CRH and ACTH secretion, whereas intermediate and delayed mechanisms mediated by genomic actions involve the modulation of limbic circuitry and peripheral metabolic messengers. Consistent with their key adaptive roles, HPA axis components are evolutionarily conserved, being present in the earliest vertebrates. An understanding of these basic mechanisms may lead to novel approaches for the development of diagnostic and therapeutic tools for disorders related to stress and alterations of GC secretion.
正常的下丘脑 - 垂体 - 肾上腺(HPA)轴活动导致肾上腺糖皮质激素(GCs)有节律地、间歇性释放,这对于机体在应激期间的内环境稳态和生存至关重要。通过大脑和外周的特定细胞内受体发挥作用,GCs调节行为以及代谢、心血管、免疫和神经内分泌活动。与慢性升高水平相反,昼夜节律性和急性应激诱导的GCs增加对于海马神经元的存活以及记忆的获取和巩固是必要的,这是由于抑制细胞凋亡、促进谷氨酸能神经传递和兴奋性突触的形成,以及诱导即刻早期基因和树突棘形成。除了导致能量可用性增加的代谢作用外,GCs主要通过调节促食欲和抑食欲神经肽对摄食行为有深远影响。越来越多的证据表明,除了通过抵消肾上腺素能促炎作用而被认可的GCs免疫抑制作用外,昼夜节律性升高在免疫系统中具有启动作用,增强急性防御反应。此外,GCs的负反馈涉及多种机制,导致HPA轴激活受限并防止过量GC产生的有害影响。满足机体需求的适当GC分泌受到控制下丘脑促肾上腺皮质激素释放激素(CRH)和血管加压素分泌的复杂神经回路的严格调节,而CRH和血管加压素是垂体促肾上腺皮质激素(ACTH)的主要调节因子。快速反馈机制可能涉及GCs的非基因组作用,介导对下丘脑CRH和ACTH分泌的即时抑制,而由基因组作用介导的中间和延迟机制涉及边缘回路和外周代谢信使的调节。与其关键的适应性作用一致,HPA轴成分在进化上是保守的,最早的脊椎动物中就已存在。对这些基本机制的理解可能会为开发与应激和GC分泌改变相关疾病的诊断和治疗工具带来新方法。