https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16517 Wed 11 Apr 2018 16:11:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12284 Wed 11 Apr 2018 12:10:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21983 Wed 11 Apr 2018 12:06:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33789 Tue 15 Jan 2019 12:58:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24307 A receptor subunits that normally heighten neurosteroid sensitivity. These stressors also result in altered placental allopregnanolone metabolism pathways. These findings suggest that reduced neurosteroid production and action in the perinatal period may contribute to some of the adverse neurodevelopmental and behavioural outcomes that result from these pregnancy compromises. Studies examining perinatal steroid supplementation therapy with non-metabolisable neurosteroid analogues to improve these outcomes are warranted.]]> Thu 21 Oct 2021 12:51:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32953 A receptor subunit composition, which may further limit neurosteroid action. The objective of this study was to determine the effects of suppression of allopregnanolone levels on the markers of development and functional outcome. Pregnant guinea pigs were treated with finasteride at a dose (25 mg/kg maternal weight) shown to suppress allopregnanolone between 60 days of gestation until delivery (term ~71 days). The cerebella from neonates, whose mothers were treated with finasteride or vehicle during pregnancy, were collected at postnatal age 8. Pups that received finasteride displayed significantly greater glial fibrillary acid protein area coverage and reduced GABA_A receptor a α₆-subunit messenger RNA within the cerebellum than pups that were exposed to vehicle. These findings indicate that loss of neurosteroid action on the foetal brain in late gestation produces prolonged astrocyte activation and reductions in GABA_A receptor a α₆-subunit expression. These changes may contribute to the long-term changes in function associated with preterm birth.]]> Thu 16 Aug 2018 13:35:57 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32951 Thu 16 Aug 2018 13:35:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7563 Sat 24 Mar 2018 08:42:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8296 Sat 24 Mar 2018 08:40:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8294 Sat 24 Mar 2018 08:40:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7900 Sat 24 Mar 2018 08:35:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:986 A receptor and suppress the fetal CNS activity. These steroids are synthesized in the fetal brain either from cholesterol or from circulating precursors derived from the placenta. The concentrations of allopregnanolone are remarkably high in the fetal brain and rise further in response to acute hypoxic stress, induced by constriction of the umbilical cord. This response may result from the increased 5α-reductase and cytochrome P-450_SCC expression in the brain. These observations suggest that the rise in neurosteroid concentrations in response to acute hypoxia may represent an endogenous protective mechanism that reduces excitotoxicity following hypoxic stress in the developing brain. In contrast to acute stress, chronic hypoxemia induces neurosteroidogenic enzyme expression without an increase in neurosteroid concentrations and, therefore, may pose a greater risk to the fetus. At birth, the allopregnanolone concentrations in the brain fall markedly, probably due to the loss of placental precursors; however, stressors, including hypoxia and endotoxin-induced inflammation, raise allopregnanolone concentrations in the newborn brain. This may protect the newborn brain from hypoxia-induced damage. However, the rise in allopregnanolone concentrations was also associated with increased sleep. This rise in sedative steroid levels may depress arousal and contribute to the risk of sudden infant death syndrome. Our recent findings indicate that acute hypoxic stress in pregnancy initiates a neurosteroid response that may protect the fetal brain from hypoxia-induced cell death, whereas the decline in allopregnanolone levels after birth may result in greater vulnerability to brain injury in neonates.]]> Sat 24 Mar 2018 08:29:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14494 Sat 24 Mar 2018 08:21:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16511 Sat 24 Mar 2018 08:04:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16519 Sat 24 Mar 2018 08:01:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16523 Sat 24 Mar 2018 08:01:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16540 Sat 24 Mar 2018 08:01:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5459 Sat 24 Mar 2018 07:48:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:6660 Sat 24 Mar 2018 07:46:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28160 Sat 24 Mar 2018 07:36:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4813 Sat 24 Mar 2018 07:20:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24848 Sat 24 Mar 2018 07:11:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37890 Fri 11 Jun 2021 09:29:09 AEST ]]>