Downregulation of Hippocampal GABA after Hypoxia-Induced Seizures in Neonatal Rats

Wang, Yanmei; Zhan, Lijun; Zeng, Wei; Li, Ke; Sun, Weiwen; Xu, Zao C.; Xu, En

doi:10.1007/s11064-011-0565-4

Cited by 31 publications

(19 citation statements)

References 45 publications

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“…It was documented that neuronal loss occurred in some neonatal seizure models, though in other animal models, such as hypoxia-induced model cell loss, it might not occur (Koh et al, 2004;Bjorkman et al, 2010;Dunleavy et al, 2010;Baram et al, 2011;Wang et al, 2011). Therefore, hypoxia-induced neonatal seizures may be not sufficient to induce hippocampal damage.…”

Section: Effects Of Hypoxia-induced Neonatal Seizures On Mfs and Neurmentioning

confidence: 99%

“…Additionally, a recent study raised a safety concern regarding the potential deleterious effects of bumetanide on immature brains, and challenged the promising therapeutic efficacy for the long-term treatment of neonatal seizures (Wang et al, 2011). It should be noted that the fundamental assumption of this study was based on the experiments conducted in normal conditions during a specific critical period.…”

Section: Effects Of Hypoxia-induced Neonatal Seizures On Eeg Seizuresmentioning

confidence: 99%

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In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

Wang¹,

Zhang²,

Song³

et al. 2015

Neuroscience

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Section: Effects Of Hypoxia-induced Neonatal Seizures On Mfs and Neurmentioning

confidence: 99%

Section: Effects Of Hypoxia-induced Neonatal Seizures On Eeg Seizuresmentioning

confidence: 99%

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

Wang¹,

Zhang²,

Song³

et al. 2015

Neuroscience

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“…Cell counts were conducted by densities as previously described (17). Cell counts were conducted by densities as previously described (17).…”

Section: Assessment Of Cellular Damagementioning

confidence: 99%

Hypoxia-Inducible Factor 1α Mediates Neuroprotection of Hypoxic Postconditioning Against Global Cerebral Ischemia

Zhu¹,

Zhan²,

Liang³

et al. 2014

J Neuropathol Exp Neurol

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Hypoxia administered after transient global cerebral ischemia (tGCI) has been shown to induce neuroprotection in adult rats, but the underlying mechanisms for this protection are unclear. Here, we tested the hypothesis that hypoxic postconditioning (HPC) induces neuroprotection through upregulation of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF), and that this involves phosphatidylinositol-3-kinase (PI3K), p38 mitogen-activated protein kinase (p38 MAPK), and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) pathways. The expression of HIF-1α, VEGF, and cleaved caspase-9 were determined by immunohistochemistry and Western blot. As pharmacologic interventions, the HIF-1α inhibitor 2-methoxyestradiol (2ME2), PI3K inhibitor LY294002, p38 MAPK inhibitor SB203580, and MEK inhibitor U0126 were administered before HPC or after tGCI. We found that HPC maintained the higher expression of HIF-1α and VEGF and decreased cleaved caspase-9 levels in CA1 after tGCI. These effects were reversed by 2ME2 administered before HPC, and the neuroprotection of HPC was abolished. LY294002 and SB203580 decreased the expression of HIF-1α and VEGF after HPC, whereas U0126 increased HIF-1α and VEGF after tGCI. These findings suggested that HIF-1α exerts neuroprotection induced by HPC against tGCI through VEGF upregulation and cleaved caspase-9 downregulation, and that the PI3K, p38 MAPK, and MEK pathways are involved in the regulation of HIF-1α and VEGF.

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“…For example, PVIs in the striatum are sensitive to 6-hydroxydopamine (Salin et al, 2009), quinolic acid (Giampà et al, 2006), rotenone (Lapointe et al, 2004), and methamphetamine (Zhu et al, 2006) and developmental injections of 3-nitropropionic acid (3-NP) cause a long-term loss of PV protein (Gibson and Clowry, 2003). Of particular interest is the vulnerability of cortical, hippocampal, and striatal PVIs to perinatal anoxia/hypoxia (Dell’Anna et al, 1996; Van de Berg et al, 2003; Gerstein et al, 2005; Wang et al, 2011) and global ischemia (Guan et al, 2000; Meade et al, 2000), considering that perinatal complications and/or hypoxia could be significant environmental factors contributing to the development of schizophrenia.…”

Section: Pv Interneuron-specific Vulnerability To Oxidative Stressmentioning

confidence: 99%

Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia

Jiang¹,

Cowell²,

Nakazawa³

2013

Front. Behav. Neurosci.

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Schizophrenia etiology is thought to involve an interaction between genetic and environmental factors during postnatal brain development. However, there is a fundamental gap in our understanding of the molecular mechanisms by which environmental factors interact with genetic susceptibility to trigger symptom onset and disease progression. In this review, we summarize the most recent findings implicating oxidative stress as one mechanism by which environmental insults, especially early life social stress, impact the development of schizophrenia. Based on a review of the literature and the results of our own animal model, we suggest that environmental stressors such as social isolation render parvalbumin-positive interneurons (PVIs) vulnerable to oxidative stress. We previously reported that social isolation stress exacerbates many of the schizophrenia-like phenotypes seen in a conditional genetic mouse model in which NMDA receptors (NMDARs) are selectively ablated in half of cortical and hippocampal interneurons during early postnatal development (Belforte et al., 2010). We have since revealed that this social isolation-induced effect is caused by impairments in the antioxidant defense capacity in the PVIs in which NMDARs are ablated. We propose that this effect is mediated by the down-regulation of PGC-1α, a master regulator of mitochondrial energy metabolism and anti-oxidant defense, following the deletion of NMDARs (Jiang et al., 2013). Other potential molecular mechanisms underlying redox dysfunction upon gene and environmental interaction will be discussed, with a focus on the unique properties of PVIs.

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Downregulation of Hippocampal GABA after Hypoxia-Induced Seizures in Neonatal Rats

Cited by 31 publications

References 45 publications

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

Hypoxia-Inducible Factor 1α Mediates Neuroprotection of Hypoxic Postconditioning Against Global Cerebral Ischemia

Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia

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