کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4332233 1292891 2006 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Regulation of forebrain GABAergic stress circuits following lesion of the ventral subiculum
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Regulation of forebrain GABAergic stress circuits following lesion of the ventral subiculum
چکیده انگلیسی

Ventral subiculum (vSUB) lesions enhance corticosterone responses to psychogenic stressors via trans-synaptic influences on paraventricular nucleus (PVN) neurons. Synaptic relays likely occur in GABA-rich regions interconnecting the vSUB and PVN. The current study examines whether vSUB lesions compromise stress-induced c-fos induction and GABA biosynthetic capacity in putative limbic–hypothalamic stress relays. Male Sprague–Dawley rats received bilateral ibotenate or sham lesions of the vSUB. Animals were divided into two groups, with one group receiving exposure to novelty stress and the other left unstressed. Exposure to novelty stress increased c-fos mRNA expression in the PVN to a greater degree in vSUB lesion relative to shams, consistent with an inhibitory role for the vSUB in the HPA stress response. However, c-fos induction was not affected in other forebrain GABAergic stress pathways, such as the lateral septum, medial preoptic area or dorsomedial hypothalamus. vSUB lesions increased GAD65 or GAD67 mRNA levels in several efferent targets, including anterior and posterior subnuclei of the bed nucleus of the stria terminalis and lateral septum. Lesions did not effect stress-induced increases in GAD65 expression in principal output nuclei of the amygdala. The current data suggest that loss of vSUB innervations produces a compensatory increase in GAD expression in subcortical targets; however, this up-regulation is insufficient to block lesion-induced stress hyperresponsiveness, perhaps driven by amygdalar disinhibition of the PVN.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1116, Issue 1, 20 October 2006, Pages 132–142
نویسندگان
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