https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Betamethasone: a neuroactive steroid deficit and adverse effects in the brain? https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:6907 Wed 11 Apr 2018 16:26:58 AEST ]]> Reduced neurosteroid exposure following preterm birth and its' contribution to neurological impairment: a novel avenue for preventative therapies https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36900 Wed 02 Mar 2022 14:24:28 AEDT ]]> Administration of progesterone throughout pregnancy increases maternal steroids without adverse effect on mature oligodendrocyte immunostaining in the guinea pig https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36998 Thu 30 Jul 2020 16:59:13 AEST ]]> Cellular distribution of the GABAᴀ receptor-modulating 3α-hydroxy, 5α-reduced pregnane steroids in the adult rat brain https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7563 Sat 24 Mar 2018 08:42:03 AEDT ]]> Effect of maternal administration of allopregnanolone before birth asphyxia on neonatal hippocampal function in the spiny mouse https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16516 A receptor, and that has anti-apoptotic and anti-excitotoxic actions, reducing brain damage in adult animal models of brain injury. We sought to determine if prophylactic treatment of the pregnant female with a single dose of this steroid could reduce birth asphyxia-induced losses in hippocampal function at 5 days of age (P5) in spiny mouse neonates (Acomys cahirinus). At 37 days gestation (term = 39 days) and 1 h before inducing birth asphyxia, spiny mice dams were injected subcutaneously (0.2 ml) with either 3 mg/kg allopregnanolone or 20% w/v β-cyclodextrin vehicle. One hour later, fetuses were either delivered immediately by caesarean section (control group) or exposed to 7.5 min of in utero asphyxia, causing acidosis and hypoxia. At P5, ex vivo hippocampal plasticity was assessed, or brains collected to determine cell proliferation (proliferating cell nuclear antigen; PCNA) or calcium channel expression (inositol trisphosphate receptor type 1; IP₃R1) using immunohistochemistry. Allopregnanolone partially prevented the decrease in long term potentiation at P5, and the asphyxia-induced increase in IP₃R1 expression in CA1 pyramidal neurons. There was no effect of allopregnanolone on the asphyxia induced impairment of the input/output (I/O) curve and paired-pulse facilitation (PPF). In control birth pups, maternal allopregnanolone treatment caused significant changes in short term post-synaptic plasticity and also reduced hippocampal proliferation at P5. These findings show that allopregnanolone can modulate hippocampal development and synaptic function in a normoxic or hypoxic environment, possibly by modifying calcium metabolism. Best practice for treatment dose and timing of treatment will need to be carefully considered.]]> Sat 24 Mar 2018 08:01:15 AEDT ]]> Models of perinatal compromises in the guinea pig: their use in showing the role of neurosteroids in pregnancy and the newborn https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29502 Sat 24 Mar 2018 07:29:45 AEDT ]]> A tale of two steroids: the importance of the androgens DHEA and DHEAS for early neurodevelopment https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45493 Fri 28 Oct 2022 15:53:26 AEDT ]]> Effects of prenatal stress on fetal neurodevelopment and responses to maternal neurosteroid treatment in guinea pigs https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16551 Fri 16 Aug 2024 13:21:52 AEST ]]>