Mironova Vera, Rybnikova E, Pivina S
Russian Academy of Sciences Laboratory of Neuroendocrinology, I. P. Pavlov Institute of Physiology Makarova 6 St. Petersburg 199034 Russian Federation.
Acta Physiol Hung. 2013 Dec;100(4):395-410. doi: 10.1556/APhysiol.100.2013.4.4.
The present study was designed to reveal possible common and specific neuroendocrine mechanisms of depression and anxiety-like states in rodents. Animal models of depression and anxiety (in particular, posttraumatic stress disorder, PTSD) were applied including the learned helplessness and the stress-restress paradigms, respectively. Immunocytochemical staining revealed that depressive- and anxiety-like states in animals were accompanied by the rise in corticotropin-releasing hormone (CRH) immunoreactivity in the parvocellular division of the hypothalamic paraventricular nucleus (PVN). Decrease in vasopressin-immunoreactivity in early period of depressive-like state development was followed by the normalization of vasopressin content in the hypothalamic PVN in delayed period. Increased CRH and vasopressin immunoreactivity in the magnocellular part of the PVN in delayed period of anxiety-like state development was detected only in the stress-restress paradigm. These results suggest that CRH hyperdrive in the parvocellular PVN appears to be a common neuroendocrine abnormality for depressive- and anxiety-like states in animals, while over-expression of CRH and vasopressin in the magnocellular PVN represents a specific feature of anxiety/PTSD-like state.
本研究旨在揭示啮齿动物抑郁和焦虑样状态可能的共同和特定神经内分泌机制。分别应用了抑郁和焦虑的动物模型（特别是创伤后应激障碍，PTSD），包括习得性无助和应激-应激范式。免疫细胞化学染色显示，动物的抑郁样和焦虑样状态伴随着下丘脑室旁核（PVN）小细胞部促肾上腺皮质激素释放激素（CRH）免疫反应性的升高。在抑郁样状态发展早期，加压素免疫反应性降低，随后在下丘脑PVN延迟期加压素含量恢复正常。仅在应激-应激范式中，在焦虑样状态发展延迟期检测到PVN大细胞部CRH和加压素免疫反应性增加。这些结果表明，小细胞PVN中CRH过度驱动似乎是动物抑郁样和焦虑样状态常见的神经内分泌异常，而大细胞PVN中CRH和加压素的过度表达代表了焦虑/PTSD样状态的特定特征。
