Herman J P, Cullinan W E, Morano M I, Akil H, Watson S J
Department of Anatomy and Neurobiology, University of Kentucky School of Medicine, Lexington 40536-0084, USA.
J Neuroendocrinol. 1995 Jun;7(6):475-82. doi: 10.1111/j.1365-2826.1995.tb00784.x.
Anatomical studies indicate that the ventral subiculum is in a prime position to mediate hippocampal inhibition of the hypothalamo-pituitary-adrenocortical (HPA) axis. The present study evaluated this hypothesis by assessing HPA function following ibotenic acid lesion of the ventral subiculum region. Rats with lesions of the ventral subiculum (vSUB) or ventral hippocampus (vHIPPO) did not show changes in basal corticosterone (CORT) secretion at either circadian peak or nadir time points when compared to sham-lesion rats (SHAM) or unoperated controls. However, rats with vSUB lesions exhibited a prolonged glucocorticoid stress response relative to all other groups. Baseline CRH mRNA levels were significantly increased in the medial parvocellular paraventricular nucleus (PVN) of the vSUB group relative to controls. CRH mRNA differences were particularly pronounced at caudal levels of the nucleus, suggesting topographic organization of vSUB interactions with PVN neurons. Notably, the vHIPPO group, which received large lesions of ventral CA1, CA3 and dentate gyrus without significant subicular damage, showed no change in stress-induced CORT secretion, suggesting that the ventral subiculum proper is principally responsible for ventral hippocampal actions on the HPA stress response. No differences in medial parvocellular PVN AVP mRNA expression were seen in either the vSUB or vHIPPO groups. The results indicate a specific inhibitory action of the ventral subiculum on HPA activation. The increase in CRH biosynthesis and stress-induced CORT secretion in the absence of changes in baseline CORT secretion or AVP mRNA expression suggests that the inhibitory actions of ventral subicular neurons affect the response capacity of the HPA axis.
解剖学研究表明，腹侧下托处于介导海马体对下丘脑 - 垂体 - 肾上腺皮质（HPA）轴抑制作用的关键位置。本研究通过评估腹侧下托区域注射鹅膏蕈氨酸损伤后的HPA功能来验证这一假设。与假手术大鼠（SHAM）或未手术对照组相比，腹侧下托（vSUB）或腹侧海马体（vHIPPO）损伤的大鼠在昼夜高峰或最低点时间点的基础皮质酮（CORT）分泌均未出现变化。然而，与所有其他组相比，vSUB损伤的大鼠表现出糖皮质激素应激反应延长。相对于对照组，vSUB组内侧小细胞室旁核（PVN）的基线促肾上腺皮质激素释放激素（CRH）mRNA水平显著升高。CRH mRNA差异在该核的尾侧水平尤为明显，表明vSUB与PVN神经元的相互作用存在拓扑组织。值得注意的是，vHIPPO组接受了腹侧CA1、CA3和齿状回的大面积损伤但未出现明显的下托损伤，其应激诱导的CORT分泌没有变化，这表明腹侧下托本身主要负责腹侧海马体对HPA应激反应的作用。在vSUB或vHIPPO组中，内侧小细胞PVN的精氨酸加压素（AVP）mRNA表达均未发现差异。结果表明腹侧下托对HPA激活具有特定的抑制作用。在基线CORT分泌或AVP mRNA表达无变化的情况下，CRH生物合成增加和应激诱导的CORT分泌增加表明腹侧下托神经元的抑制作用影响了HPA轴的反应能力。
