ArticleNeuropharmacology2009
Post-hypoxic changes in rat cortical neuron GABA A receptor function require L-type voltage-gated calcium channel activation.
Article in Neuropharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Imbalance of Essential Metals in Traumatic Brain Injury and Its Possible Link with Disorders of Consciousness.International journal of molecular sciences · 2023Review
- Intermittent hypoxia: linkage between OSAS and epilepsy.Frontiers in pharmacology · 2023Review
- Regulation of GABAMembranes · 2021Review
- A lab-on-a-chip for hypoxic patch clamp measurements combined with optical tweezers and spectroscopy- first investigations of single biological cells.Biomedical engineering online · 2015Article
- Hypoxia enhances high-voltage-activated calcium currents in rat primary cortical neurons via calcineurin.Epilepsy research · 2012Article
- Traumatic brain injury and the effects of diazepam, diltiazem, and MK-801 on GABA-A receptor subunit expression in rat hippocampus.Journal of biomedical science · 2010Article
- Chronic benzodiazepine-induced reduction in GABA(A) receptor-mediated synaptic currents in hippocampal CA1 pyramidal neurons prevented by prior nimodipine injection.Neuroscience · 2008Article
- Expression levels of the alpha4 subunit of the GABA(A) receptor in differentiated neuroblastoma cells are correlated with GABA-gated current.NeuropharmacologyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hypoxia modifies GABA(A) receptor (GABA(A)R) function and can cause seizures, encephalopathy or myoclonus. To characterize the effects of hypoxia on neuronal GABA(A)Rs, we subjected rat cortical neurons to 1% O2 for 2, 4 or 8h, followed by recovery times of 0-96h, and used whole-cell and perforated patch-clamp recording to assess GABA(A)R currents and pharmacology. Hypoxic exposure for 4h caused downregulation of maximal GABA current immediately following hypoxia and after 48h recovery without changing the EC50 for GABA. Two- and eight-hour hypoxic exposures had inconsistent effects on GABA(A)R currents. Maximal diazepam potentiation was increased immediately following 4h hypoxia, while potentiation by zolpidem was increased after 48h recovery. Pentobarbital enhancement and zinc inhibition of GABA currents were unchanged. Hypoxia also caused a depolarizing shift in the reversal potential of GABA-induced Cl(-) currents after 24h recovery. The L-type voltage-gated calcium channel (L-VGCC) blocker, nitrendipine, during hypoxia or control treatment prevented the reduction in GABA(A)R currents, and increased control currents over baseline. Nitrendipine also prevented the increase in zolpidem potentiation 48h after hypoxia, and blocked the depolarizing shift in Cl(-) reversal potential 24h after hypoxia. The effects of hypoxia on maximal GABA(A)R currents, zolpidem pharmacology and Cl(-) reversal potential thus require depolarization-induced calcium entry via L-VGCCs, and constitutive L-VGCC activity appears to reduce maximal GABA(A)R currents in control neurons via a calcium-dependent process. Calcium-dependent modulation of GABA(A)R currents via L-VGCCs may be a fundamental regulatory mechanism for GABA receptor function.
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Registered trials
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