https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54326 Wed 28 Feb 2024 15:19:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25334 Wed 11 Apr 2018 15:03:48 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4430 Wed 11 Apr 2018 13:56:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15128 Wed 11 Apr 2018 12:22:53 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12630 Wed 11 Apr 2018 10:07:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16611 0.001). Trends in receptor binding site density measurements supported this observation (P = 0.07). Glucocorticoid exposure increased β₁-adrenoceptor mRNA levels in the right ventricle of preterm hearts (P = 0.008) but did not alter expression in the left ventricle (P>0.1). Relative abundance of a1A-adrenoceptor mRNA was the same in preterm and term piglet hearts (P = >0.1) but was reduced by maternal glucocorticoid treatment (P<0.01); a2A-adrenoceptor mRNA abundance was higher in untreated and glucocorticoid exposed preterm piglet hearts than in term piglets (P<0.001). There was no difference between male and female piglets in mRNA abundance of any of the genes studied. In conclusion, there is reduced mRNA abundance of β₁-adrenoceptors in the preterm pig heart. If this lower expression of β-adrenoceptors occurs in human preterm infants, it could explain their poor cardiovascular function and their frequent failure to respond to commonly used inotropes.]]> Wed 11 Apr 2018 09:23:09 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8116 Sat 24 Mar 2018 08:40:01 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9573 Sat 24 Mar 2018 08:34:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10912 Sat 24 Mar 2018 08:07:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18322 Sat 24 Mar 2018 08:04:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17775 A receptors, high K⁺, DA receptors) also increased or decreased cellular TH immunoreactivity but decreased or increased, respectively, the number of TH+ cells in SNc. We conclude that in adult SNc neurons: (i) TH expression is activity-dependent and begins to change ~20 h following sustained changes in neuronal activity; (ii) ion-channels and receptors mediating cell-autonomous activity or synaptic input are equally potent in altering TH expression; and (iii) activity-dependent changes in TH expression are balanced by opposing changes in the number of TH+ SNc cells.]]> Sat 24 Mar 2018 07:57:41 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21373 Sat 24 Mar 2018 07:51:27 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5208 Sat 24 Mar 2018 07:47:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49704 Mon 29 May 2023 13:00:55 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32284 Mon 23 Sep 2019 10:58:58 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33142 Mon 03 Sep 2018 12:55:09 AEST ]]>