ArticleNeuropharmacology2009
Ischaemia differentially regulates GABA(B) receptor subunits in organotypic hippocampal slice cultures.
Article in Neuropharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Transient plasticity response is regulated by histone deacetylase inhibitor in oxygen-glucose deprivation condition.Pharmacological reports : PR · 2023Article
- Targeting the Interaction of GABAFrontiers in pharmacology · 2022Article
- Sustained Baclofen-Induced Activation of GABAFrontiers in molecular neuroscience · 2021Article
- The Effects of GABAergic System under Cerebral Ischemia: Spotlight on Cognitive Function.Neural plasticity · 2020Review
- Activity-dependent plasticity of presynaptic GABASynapse (New York, N.Y.) · 2018Article
- Acute death of astrocytes in blast-exposed rat organotypic hippocampal slice cultures.PloS one · 2017Article
- Phospho-dependent Accumulation of GABABRs at Presynaptic Terminals after NMDAR Activation.Cell reports · 2016Article
- Opposing needling promotes behavior recovery and exerts neuroprotection via the cAMP/PKA/CREB signal transduction pathway in transient MCAO rats.Molecular medicine reports · 2016Article
- Baclofen mediates neuroprotection on hippocampal CA1 pyramidal cells through the regulation of autophagy under chronic cerebral hypoperfusion.Scientific reports · 2015Article
- Cross-talk and regulation between glutamate and GABAB receptors.Frontiers in cellular neuroscience · 2015Review
- Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury.Scientific reports · 2014Article
- Calcium-sensing receptor (CaSR) as a novel target for ischemic neuroprotection.Annals of clinical and translational neurology · 2014Article
- Activation of GABAB receptors ameliorates cognitive impairment via restoring the balance of HCN1/HCN2 surface expression in the hippocampal CA1 area in rats with chronic cerebral hypoperfusion.Molecular neurobiology · 2014Article
- Ischemia-like oxygen and glucose deprivation mediates down-regulation of cell surface γ-aminobutyric acidB receptors via the endoplasmic reticulum (ER) stress-induced transcription factor CCAAT/enhancer-binding protein (C/EBP)-homologous protein (CHOP).The Journal of biological chemistry · 2014Article
- Differential regulation of GABAB receptor trafficking by different modes of N-methyl-D-aspartate (NMDA) receptor signaling.The Journal of biological chemistry · 2014Article
- Role of the axonal initial segment in psychiatric disorders: function, dysfunction, and intervention.Frontiers in psychiatry · 2014Review
- Modulation of cell surface GABA(B) receptors by desensitization, trafficking and regulated degradation.World journal of biological chemistry · 2012Article
- Sustained glutamate receptor activation down-regulates GABAB receptors by shifting the balance from recycling to lysosomal degradation.The Journal of biological chemistry · 2010Article
- Prolonged activation of NMDA receptors promotes dephosphorylation and alters postendocytic sorting of GABAB receptors.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- NMDA receptor-dependent GABAB receptor internalization via CaMKII phosphorylation of serine 867 in GABAB1.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Reduced synaptic inhibition due to dysfunction of ionotropic GABA(A) receptors has been proposed as one factor in cerebral ischaemia-induced excitotoxic cell death. However, the participation of the inhibitory metabotropic GABA(B) receptors in these pathological processes has not been extensively investigated. We used oxygen-glucose deprivation (OGD) and NMDA-induced excitotoxicity as models to investigate whether ischaemia-like challenges alter the protein levels of GABA(B1) and GABA(B2) receptor subunits in rat organotypic hippocampal slice cultures. Twenty-four hours after the insult both OGD and NMDA produced a marked decrease in the total levels of GABA(B2) (approximately 75%), while there was no significant change in the levels of GABA(B1) after OGD, but an increase after NMDA treatment (approximately 100%). The GABA(B) receptor agonist baclofen (100 microM) was neuroprotective following OGD or NMDA treatment if added before or during the insult. GABA(B) receptors comprise heterodimers of GABA(B1) and GABA(B2) subunits and our results suggest that the separate subunits are independently regulated in response to extreme neuronal stress. However, because GABA(B2) is required for functional surface expression, down-regulation of this subunit removes an important inhibitory feedback mechanism under pathological conditions.
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