Barakat Y, Pape J R, Boutahricht M, El Ouezzani S, Alaoui A, Chaigniau M, Tramu G, Magoul R
Laboratory of Neuroendocrinology and Nutritional and Climatic Environment, University Sidi Mohamed Ben Abdellah, Faculty of Sciences Dhar-Mehraz, Fez-Atlas, Morocco.
J Neuroendocrinol. 2006 Oct;18(10):767-75. doi: 10.1111/j.1365-2826.2006.01474.x.
The hypothalamic response to an environmental stress implicates the corticotrophin-releasing hormone (CRH) neuroendocrine system of the hypothalamic parvicellular paraventricular nucleus (PVN) in addition to other neuropeptides coexpressed within CRH neurones and controlling the hypothalamo-pituitary-adrenal (HPA) axis activity as well. Such neuropeptides are vasopressin, neurotensin and cholecystokinin (CCK). It has previously been demonstrated that the majority of the CRH neuronal population coexpresses CCK after a peripheral stress in rats. In the present study, we explored such neuroendocrine plasticity in the jerboa in captivity as another animal model. In particular, we studied CCK and CRH expression within the hypothalamic PVN by immunocytochemistry in control versus acute immobilisation stress-submitted jerboas. The results show that CCK- and CRH-immunoreactive neuronal systems are located in the hypothalamic parvicellular PVN. The number of CCK-immunoreactive neurones within the PVN was significantly increased (138% increase) in stressed animals compared to controls. Similarly, the number of CRH-containing neurones was higher in stressed jerboas (128%) compared to controls. These results suggest that the neurogenic stress caused by immobilisation stimulates CCK as well as CRH expression in jerboas, which correlates well with previous data obtained in rats using other stressors. The data obtained also suggest that, in addition to CRH, CCK is another neuropeptide involved in the response to stress in jerboa, acting by controlling HPA axis activity. Because CCK is involved in the phenotypical plasticity of CRH-containing neurones in response to an environmental stress, we also explored their coexpression by double immunocytochemistry within the PVN and the median eminence (i.e. the site of CRH and CCK corelease in the rat) following jerboa immobilisation. The results show that CCK is not coexpressed within CRH neurones in either control or stressed jerboa, suggesting differences between jerboas and rats in the neuroendocrine regulatory mechanisms of the stress response involving CRH and CCK. The adaptative physiological mechanisms to environmental conditions might vary from one mammal species to another.
下丘脑对环境应激的反应涉及下丘脑小细胞室旁核（PVN）的促肾上腺皮质激素释放激素（CRH）神经内分泌系统，此外还有与CRH神经元共表达且同样控制下丘脑 - 垂体 - 肾上腺（HPA）轴活动的其他神经肽。这类神经肽包括血管加压素、神经降压素和胆囊收缩素（CCK）。此前已证实，在大鼠受到外周应激后，大多数CRH神经元群体共表达CCK。在本研究中，我们以圈养的跳鼠作为另一种动物模型，探索了这种神经内分泌可塑性。具体而言，我们通过免疫细胞化学方法，研究了对照跳鼠与经受急性固定应激的跳鼠下丘脑PVN内CCK和CRH的表达情况。结果显示CCK免疫反应性和CRH免疫反应性神经元系统位于下丘脑小细胞PVN。与对照组相比，应激动物PVN内CCK免疫反应性神经元数量显著增加（增加了138%）。同样，应激跳鼠中含CRH神经元的数量比对照组高（128%）。这些结果表明，固定引起的神经源性应激刺激了跳鼠体内CCK和CRH的表达，这与先前在大鼠中使用其他应激源获得的数据高度相关。所获得的数据还表明，除了CRH之外，CCK是另一种参与跳鼠应激反应的神经肽，通过控制HPA轴活动发挥作用。由于CCK参与含CRH神经元对环境应激的表型可塑性，我们还通过双重免疫细胞化学方法，研究了跳鼠固定后PVN和正中隆起（即大鼠中CRH和CCK共同释放的部位）内它们的共表达情况。结果显示，在对照或应激跳鼠的CRH神经元内，CCK均不共表达，这表明在涉及CRH和CCK的应激反应神经内分泌调节机制方面，跳鼠与大鼠存在差异。对环境条件的适应性生理机制可能因哺乳动物物种而异。
