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10.3389/fendo.2016.00137 http://scihub22266oqcxt.onion/10.3389/fendo.2016.00137 C5086584!5086584 !27843437     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27843437 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Endocrinol+(Lausanne) 2016 ; 7 (ä): 137 Nephropedia Template TP {{tp|p=27843437 |t=2016. Paraventricular Hypothalamic Mechanisms of Chronic Stress Adaptation |pdf=|usr=}}{{27843437 }} gab.com Text Paraventricular Hypothalamic Mechanisms of Chronic Stress Adaptation JO: Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=27843437 #FOAvip The hypothalamic paraventricular nucleus (PVN) is the primary driver of hypothalamo-pituitary-adrenocortical (HPA) responses. At least part of the role of the PVN is managing the demands of chronic stress exposure. With repeated exposure to stress, hypophysiotrophic corticotropin-releasing hormone (CRH) neurons of the PVN display a remarkable cellular, synaptic, and connectional plasticity that serves to maximize the ability of the HPA axis to maintain response vigor and flexibility. At the cellular level, chronic stress enhances the production of CRH and its co-secretagogue arginine vasopressin and rearranges neurotransmitter receptor expression so as to maximize cellular excitability. There is also evidence to suggest that efficacy of local glucocorticoid feedback is reduced following chronic stress. At the level of the synapse, chronic stress enhances cellular excitability and reduces inhibitory tone. Finally, chronic stress causes a structural enhancement of excitatory innervation, increasing the density of glutamate and noradrenergic/adrenergic terminals on CRH neuronal cell somata and dendrites. Together, these neuroplastic changes favor the ability of the HPA axis to retain responsiveness even under conditions of considerable adversity. Thus, chronic stress appears able to drive PVN neurons via a number of convergent mechanisms, processes that may play a major role in HPA axis dysfunction seen in variety of stress-linked disease states. Twit Text FOAVip Paraventricular Hypothalamic Mechanisms of Chronic Stress Adaptation ????Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=27843437 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27843437 #FOAvip English Wikipedia <ref>{{Cite pmid|27843437 }}</ref> Paraventricular Hypothalamic Mechanisms of Chronic Stress Adaptation #MMPMID27843437 Herman JP ; Tasker JG Front Endocrinol (Lausanne) 2016[]; 7 (ä): 137 PMID27843437 show ga The hypothalamic paraventricular nucleus (PVN) is the primary driver of hypothalamo-pituitary-adrenocortical (HPA) responses. At least part of the role of the PVN is managing the demands of chronic stress exposure. With repeated exposure to stress, hypophysiotrophic corticotropin-releasing hormone (CRH) neurons of the PVN display a remarkable cellular, synaptic, and connectional plasticity that serves to maximize the ability of the HPA axis to maintain response vigor and flexibility. At the cellular level, chronic stress enhances the production of CRH and its co-secretagogue arginine vasopressin and rearranges neurotransmitter receptor expression so as to maximize cellular excitability. There is also evidence to suggest that efficacy of local glucocorticoid feedback is reduced following chronic stress. At the level of the synapse, chronic stress enhances cellular excitability and reduces inhibitory tone. Finally, chronic stress causes a structural enhancement of excitatory innervation, increasing the density of glutamate and noradrenergic/adrenergic terminals on CRH neuronal cell somata and dendrites. Together, these neuroplastic changes favor the ability of the HPA axis to retain responsiveness even under conditions of considerable adversity. Thus, chronic stress appears able to drive PVN neurons via a number of convergent mechanisms, processes that may play a major role in HPA axis dysfunction seen in variety of stress-linked disease states. äParaventricular Hypothalamic Mechanisms of Chronic Stress Adaptation (epmc).pdf DeepDyve Pubget Overpricing