ArticleThe Journal of physiology2007
GABA transient sets the susceptibility of mIPSCs to modulation by benzodiazepine receptor agonists in rat hippocampal neurons.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Brainwaves under medication: revealing class-specific neural signatures of psychotropic medication from 24,000 EEGs.EBioMedicine · 2026Article
- Φ value analysis underscores strong functional and structural compactness of the GABAProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Chronic benzodiazepine treatment triggers gephyrin scaffold destabilization and GABAFrontiers in cellular neuroscience · 2025Article
- Inhibitory and excitatory synaptic neuroadaptations in the diazepam tolerant brain.Neurobiology of disease · 2023Article
- Benzodiazepine Modulation of GABABiomolecules · 2022Review
- Mutations at the M2 and M3 Transmembrane Helices of the GABAACS chemical neuroscience · 2021Article
- αACS chemical neuroscience · 2021Article
- Midazolam: an essential palliative care drug.Palliative care and social practice · 2020Review
- Looking for Novelty in an "Old" Receptor: Recent Advances Toward Our Understanding of GABAFrontiers in neuroscience · 2020Review
- GABAFrontiers in cellular neuroscience · 2020Article
- Distinct Modulation of Spontaneous and GABA-Evoked Gating by Flurazepam Shapes Cross-Talk Between Agonist-Free and Liganded GABAFrontiers in cellular neuroscience · 2018Article
- Benzodiazepine treatment induces subtype-specific changes in GABA(A) receptor trafficking and decreases synaptic inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Influence of GABAAR monoliganded states on GABAergic responses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Impact of synaptic neurotransmitter concentration time course on the kinetics and pharmacological modulation of inhibitory synaptic currents.Frontiers in cellular neuroscience · 2011Article
- Is attentional blink a byproduct of neocortical attractors?Frontiers in computational neuroscience · 2011Article
- Phenobarbital but Not Diazepam Reduces AMPA/kainate Receptor Mediated Currents and Exerts Opposite Actions on Initial Seizures in the Neonatal Rat Hippocampus.Frontiers in cellular neuroscience · 2011Article
- Efficient maximum likelihood estimation of kinetic rate constants from macroscopic currents.PloS one · 2011Article
- Slow GABA transient and receptor desensitization shape synaptic responses evoked by hippocampal neurogliaform cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Block and allosteric modulation of GABAergic currents by oenanthotoxin in rat cultured hippocampal neurons.British journal of pharmacology · 2010Article
- Selective induction of astrocytic gliosis generates deficits in neuronal inhibition.Nature neuroscience · 2010Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Benzodiazepines (BDZs) are known to increase the amplitude and duration of IPSCs. Moreover, at low [GABA], BDZs strongly enhance GABAergic currents suggesting the up-regulation of agonist binding while their action on gating remains a matter of debate. In the present study we have examined the impact of flurazepam and zolpidem on mIPSCs by investigating their effects on GABA(A)R binding and gating and by considering dynamic conditions of synaptic receptor activation. Flurazepam and zolpidem enhanced the amplitude and prolonged decay of mIPSCs. Both compounds strongly enhanced responses to low [GABA] but, surprisingly, decreased the currents evoked by saturating or half-saturating [GABA]. Analysis of current responses to ultrafast GABA applications indicated that these compounds enhanced binding and desensitization of GABA(A) receptors. Flurazepam and zolpidem markedly prolonged deactivation of responses to low [GABA] but had almost no effect on deactivation at saturating or half-saturating [GABA]. Moreover, at low [GABA], flurazepam enhanced desensitization-deactivation coupling but zolpidem did not. Recordings of responses to half-saturating [GABA] applications revealed that appropriate timing of agonist exposure was sufficient to reproduce either a decrease or enhancement of currents by flurazepam or zolpidem. Recordings of currents mediated by recombinant ('synaptic') alpha1beta2gamma2 receptors reproduced all major findings observed for neuronal GABA(A)Rs. We conclude that an extremely brief agonist transient renders IPSCs particularly sensitive to the up-regulation of agonist binding by BDZs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.