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The paraventricular nucleus of the hypothalamus (PVN) regulates neuroendocrine, autonomic and cardiovascular responses to stress. Stressors activate catacholaminergic systems which consequently modulates activity of organism via adrenergic receptors (ARs). Our work was focused on investigation of changes in gene expression of epinephrine-synthesizing enzyme phenylethanolamine-N-methyltransferase (PNMT), neuropeptide Y (NPY) and adrenoceptors in the heart of sham-operated and PVN-deafferentated rats exposed to immobilization stress (IMO). PNMT and NPY mRNA levels in the heart of sham-operated rats were not signifi cantly increased after a single IMO. However, posterolateral deafferentation of the PVN reduced PNMT mRNA, whereas levels of NPY mRNA were elevated. These data suggest a stimulatory role of PVN on PNMT and an inhibitory role on NPY gene expression. Moreover, β1-AR mRNA levels were signifi cantly reduced in heart of PVN-deafferentated animals comparing to sham-operated rats. On other side, after single IMO β1-AR mRNA levels were signifi cantly increased in PVN-deafferentated rats. Gene expression of other ARs (β2, β3, α1B) in hearts of stressed PVN-deafferentated animals were decreased. The found down-regulation of gene expression of ARs might suggest a rise in sympathetic activity induced by PVN deafferentation. Our data suggest that PVN plays an important role in stress-induced activation of cardiac sympathetic system.
This study explores the quantitative patterns of immunolabeled Fos protein incidence in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) oxytocinergic (OXY) neurons in response to immobilization (IMO) stress in corticotrophin releasing hormone deficient (CRH-KO) mice. Adult male mice, taken directly from cages or 120 min after a single IMO, were sacrificed by intracardial perfusion with fixative. Coronal brain sections of 30 µm thickness were processed for dual Fos/OXY immunohistochemistry. In control wild type (WT) and CRH-KO mice, scattered Fos immunoreactivity was observed in hypothalamus, including the PVN where scanty Fos signal occurred in both parvocellular and magnocellular PVN subdivisions. Dual Fos/OXY immunostainings revealed higher basal Fos expression in the PVN of control CRH-KO mice. IMO evoked a marked rise in Fos expression in OXY neurons of the PVN and SON in both WT and CRH-KO groups of mice. The present data demonstrate that 1/ CRH deficiency upregulates the basal activity of hypothalamic PVN OXY cells in CRH-KO mice and 2/ IMO stress in both WT and CRH-KO mice affects distinctly the activity of OXY cells in both SON and PVN. Our data indicate that CRH deficiency does not alter the responsiveness of PVN and SON OXY cells to IMO stress.
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