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首页> 外文期刊>The European Journal of Neuroscience >Role of paraventricular nucleus-projecting norepinephrine/epinephrine neurons in acute and chronic stress
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Role of paraventricular nucleus-projecting norepinephrine/epinephrine neurons in acute and chronic stress

机译：室旁核投射去甲肾上腺素/肾上腺素神经元在急慢性应激中的作用

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Chronic variable stress (CVS) exposure modifies the paraventricular nucleus of the hypothalamus (PVN) in a manner consistent with enhanced central drive of the hypothalamo-pituitary-adrenocortical (HPA) axis. As previous reports suggest that post-stress enhancement of norepinephrine (NE) action contributes to chronic stress regulation at the level of the PVN, we hypothesised that PVN-projecting NE neurons were necessary for the stress facilitatory effects of CVS. Following intra-PVN injection of saporin toxin conjugated to a dopamine beta-hydroxylase (DBH) antibody (DSAP), in rats PVN DBH immunoreactivity was almost completely eliminated, but immunoreactive afferents to other key regions involved in stress integration were spared (e.g. DBH fiber densities were unaffected in the central nucleus of the amygdala). Reductions in DBH-positive fiber density were associated with reduced numbers of DBH-immunoreactive neurons in the nucleus of the solitary tract and locus coeruleus. Following 2 weeks of CVS, DSAP injection did not alter stress-induced adrenal hypertrophy or attenuation of body weight gain, indicating that PVN-projecting NE [and epinephrine (E)] neurons are not essential for these physiological effects of chronic stress. In response to acute restraint stress, PVN-targeted DSAP injection attenuated peak adrenocorticotrophic hormone (ACTH) and corticosterone in controls, but only attenuated peak ACTH in CVS animals, suggesting that enhanced adrenal sensitivity compensated for reduced excitatory drive of the PVN. Our data suggest that PVN-projecting NE/E neurons contribute to the generation of acute stress responses, and are required for HPA axis drive (ACTH release) during chronic stress. However, loss of NE/E drive at the PVN appears to be buffered by compensation at the level of the adrenal.
机译：慢性可变应力（CVS）暴露以与增强下丘脑-垂体-肾上腺皮质（HPA）轴的中央驱动一致的方式修饰下丘脑（PVN）的室旁核。正如以前的报道表明，压力后去甲肾上腺素（NE）作用的增强有助于在PVN水平上调节慢性压力，我们假设PVN投射的NE神经元对于CVS的压力促进作用是必需的。在PVN内注射与多巴胺β-羟化酶（DBH）抗体（DSAP）结合的沙泊菌素毒素后，大鼠PVN DBH的免疫反应性几乎被完全消除，但其他与应激整合有关的关键区域的免疫反应性传入细胞得以保留（例如DBH纤维杏仁核中央核的密度不受影响）。 DBH阳性纤维密度的减少与孤立道和蓝斑轨迹的DBH免疫反应性神经元数量减少有关。经过2周的CVS，DSAP注射并没有改变应激引起的肾上腺肥大或体重减轻，这表明投射PVN的NE [和肾上腺素（E）]神经元对于慢性应激的这些生理效应不是必需的。为了应对急性束缚应激，以PVN为靶标的DSAP注射可减轻对照组中肾上腺皮质营养激素（ACTH）和皮质酮的峰值，但仅减弱CVS动物的ACTH峰值，表明肾上腺敏感性的增强可以补偿PVN兴奋性驱动的降低。我们的数据表明，投射PVN的NE / E神经元有助于产生急性应激反应，并且在慢性应激期间HPA轴驱动（ACTH释放）是必需的。但是，PVN处NE / E驱动器的丢失似乎可以通过肾上腺水平的补偿得到缓解。

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