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10.1152/ajpregu.00210.2014 http://scihub22266oqcxt.onion/10.1152/ajpregu.00210.2014 C4269674!4269674!25354727     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Regul+Integr+Comp+Physiol 2014 ; 307 (12): R1405-12 Nephropedia Template TP {{tp|p=25354727|t=2014. Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis |pdf=|usr=}}{{25354727}} gab.com Text Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25354727 #FOAvip Animals with a history of sodium depletions exhibit increases in salt intake, a phenomenon described as the sensitization of sodium appetite. Using a novel experimental design, the present experiments investigated whether putative molecular markers of neural plasticity and changes in the message for components of the brain renin-angiotensin-aldosterone-system (RAAS) accompany the sensitization of sodium appetite. An initial set of experiments examined whether the glutamatergic N-methyl-d-aspartate receptor antagonist MK-801 would attenuate sodium appetite sensitization and prevent changes in mRNA expression associated with sensitization. Rats with repeated sodium depletions exhibited enhanced sodium appetite and mRNA expression for components of the RAAS in areas along the lamina terminalis (LT), a region of the brain that is important for the regulation of body fluid homeostasis, and these effects were significantly attenuated by MK-801 pretreatment. A second set of experiments investigated whether successive sodium depletions would elevate sodium intake and induce a pattern of fos-B staining consistent with the ?fos-B isoform in areas along the LT. The pattern of fos-B staining in the subfornical organ was consistent with the characteristics of ?fos-B expression. Specifically, fos-B/?fos-B expression was increased 4 days after the last of a series of sodium depletions, fos-B/?fos-B expression was nearly absent in control rats, and the quantity of fos-B/?fos-B staining was directly associated with a history of sodium depletions. These findings demonstrate that the sensitization of sodium appetite is associated with sustained molecular alterations in the LT that are indicative of neural plasticity and upregulation of the central RAAS. Twit Text FOAVip Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25354727 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25354727 #FOAvip English Wikipedia <ref>{{Cite pmid|25354727}}</ref> Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis #MMPMID25354727 Hurley SW; Zhang Z; Beltz TG; Xue B; Johnson AK Am J Physiol Regul Integr Comp Physiol 2014[Dec]; 307 (12): R1405-12 PMID25354727show ga Animals with a history of sodium depletions exhibit increases in salt intake, a phenomenon described as the sensitization of sodium appetite. Using a novel experimental design, the present experiments investigated whether putative molecular markers of neural plasticity and changes in the message for components of the brain renin-angiotensin-aldosterone-system (RAAS) accompany the sensitization of sodium appetite. An initial set of experiments examined whether the glutamatergic N-methyl-d-aspartate receptor antagonist MK-801 would attenuate sodium appetite sensitization and prevent changes in mRNA expression associated with sensitization. Rats with repeated sodium depletions exhibited enhanced sodium appetite and mRNA expression for components of the RAAS in areas along the lamina terminalis (LT), a region of the brain that is important for the regulation of body fluid homeostasis, and these effects were significantly attenuated by MK-801 pretreatment. A second set of experiments investigated whether successive sodium depletions would elevate sodium intake and induce a pattern of fos-B staining consistent with the ?fos-B isoform in areas along the LT. The pattern of fos-B staining in the subfornical organ was consistent with the characteristics of ?fos-B expression. Specifically, fos-B/?fos-B expression was increased 4 days after the last of a series of sodium depletions, fos-B/?fos-B expression was nearly absent in control rats, and the quantity of fos-B/?fos-B staining was directly associated with a history of sodium depletions. These findings demonstrate that the sensitization of sodium appetite is associated with sustained molecular alterations in the LT that are indicative of neural plasticity and upregulation of the central RAAS. äSensitization of sodium appetite: evidence for sustained molecular cha(epmc).pdf DeepDyve Pubget Overpricing