Dumont E C, Kinkead R, Trottier J F, Gosselin I, Drolet G
CHUL Research Centre, Neuroscience Unit and Faculté de Médecine, Université Laval, Sainte-Foy, Québec, Canada.
J Neurochem. 2000 Nov;75(5):2200-11. doi: 10.1046/j.1471-4159.2000.0752200.x.
This study tested the hypothesis that the activation pattern of enkephalinergic (ENKergic) neurons within the paraventricular nucleus of the hypothalamus (PVH) in response to psychogenic stress is identical whether in response to repeated exposure to the same stress (homotypic; immobilization) or to a novel stress (heterotypic; air jet puff). Rats were assigned to either acute or chronic immobilization stress paradigms (90 min/day for 1 or 10 days, respectively). The chronic group was then subjected to an additional 90-min session of either heterotypic or homotypic stress. A single 90-min stress session (immobilization or air jet) increased PVH-ENK heteronuclear (hn) RNA expression. In chronically stressed rats, exposure to an additional stress session (whether homotypic or heterotypic) continued to stimulate ENK hnRNA expression. Acute immobilization caused a marked increase in the numbers of Fos-immunoreactive and Fos-ENK double-labeled cells in the dorsal and ventral medial parvicellular, and lateral parvicellular subdivisions of the PVH. Chronic immobilization caused an attenuated Fos response ( approximately 66%) to subsequent immobilization. In contrast, chronic immobilization did not impair ENKergic neuron activation within the PVH following homotypic or heterotypic stress. These results indicate that within the PVH, chronic psychogenic stress markedly attenuates the Fos response, whereas ENKergic neurons resist habituation, principally within the ventral neuroendocrine portion of the nucleus. This suggests an increase in ENK effect during chronic stress exposure. Homotypic (immobilization) and heterotypic (air jet) psychogenic stressors produce similar responses, including Fos, ENK-Fos, and ENK hnRNA, within each subdivision of the PVH, suggesting similar processing for painless neurogenic stimuli.
下丘脑室旁核(PVH)内脑啡肽能(ENKergic)神经元对心理性应激的激活模式,无论其是对重复暴露于相同应激(同型;固定)还是对新应激(异型;喷气),都是相同的。将大鼠分为急性或慢性固定应激范式组(分别为每天90分钟,持续1天或10天)。然后,对慢性组施加额外90分钟的异型或同型应激。单次90分钟的应激(固定或喷气)会增加PVH-ENK异核(hn)RNA表达。在慢性应激大鼠中,暴露于额外的应激(无论是同型还是异型)会持续刺激ENK hnRNA表达。急性固定导致PVH背侧和腹内侧小细胞以及外侧小细胞亚区中Fos免疫反应性和Fos-ENK双标记细胞数量显著增加。慢性固定导致对随后固定的Fos反应减弱(约66%)。相比之下,慢性固定并不损害同型或异型应激后PVH内脑啡肽能神经元的激活。这些结果表明,在PVH内,慢性心理性应激显著减弱Fos反应,而脑啡肽能神经元抵抗习惯化,主要是在该核的腹侧神经内分泌部分。这表明在慢性应激暴露期间脑啡肽效应增强。同型(固定)和异型(喷气)心理性应激源在PVH的每个亚区内产生相似的反应,包括Fos、ENK-Fos和ENK hnRNA,这表明对无痛神经源性刺激的处理相似。