ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Structural determinants of fast desensitization and desensitization-deactivation coupling in GABAa receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Correlations of receptor desensitization of gain-of-function GABRB3 variants with clinical severity.Brain : a journal of neurology · 2024Article
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- Dravet syndrome-associated mutations inBrain communications · 2021Article
- Reducing variability in motor cortex activity at a resting state by extracellular GABA for reliable perceptual decision-making.Journal of computational neuroscience · 2019Article
- Altered inhibitory synapses in de novo GABRA5 and GABRA1 mutations associated with early onset epileptic encephalopathies.Brain : a journal of neurology · 2019Article
- Etomidate Effects on Desensitization and Deactivation ofThe Journal of pharmacology and experimental therapeutics · 2019Article
- Comparison of αβδ and αβγ GABAPharmacological research · 2018Review
- Balancing tonic and phasic inhibition in hypothalamic corticotropin-releasing hormone neurons.The Journal of physiology · 2018Article
- GABA type a receptor trafficking and the architecture of synaptic inhibition.Developmental neurobiology · 2018Review
- GABAScientific reports · 2017Article
- De novo GABRG2 mutations associated with epileptic encephalopathies.Brain : a journal of neurology · 2017Article
- Article
- Differential regulation of synaptic and extrasynaptic α4 GABA(A) receptor populations by protein kinase A and protein kinase C in cultured cortical neurons.Neuropharmacology · 2016Article
- Article
- Etomidate uniquely modulates the desensitization of recombinant α1β3δ GABA(A) receptors.Neuroscience · 2015Article
- Neurosteroid interactions with synaptic and extrasynaptic GABA(A) receptors: regulation of subunit plasticity, phasic and tonic inhibition, and neuronal network excitability.Psychopharmacology · 2013Review
- Homeostatic competition between phasic and tonic inhibition.The Journal of biological chemistry · 2013Article
- The structural mechanism of the Cys-loop receptor desensitization.Molecular neurobiology · 2013Review
- An outline of desensitization in pentameric ligand-gated ion channel receptors.Cellular and molecular life sciences : CMLS · 2013Review
- Macroscopic kinetics of pentameric ligand gated ion channels: comparisons between two prokaryotic channels and one eukaryotic channel.PloS one · 2013Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Fast IPSCs in the brain are predominantly caused by presynaptic release of GABA that activates GABA(A) receptor (GABA(A)R) channels. The IPSCs are shaped by the gating and desensitization properties of postsynaptic GABA(A)Rs. Specifically, fast desensitization has been suggested to decrease IPSC amplitude and to increase IPSC duration by slowing deactivation; however, the mechanisms underlying desensitization, deactivation, and their coupling are poorly understood. Consistent with this suggestion, alpha1beta3gamma2L GABA(A)Rs desensitize with a prominent fast phase and deactivate slowly, whereas alpha1beta3delta GABA(A)Rs desensitize without a fast phase and deactivate rapidly. Using the concentration-jump technique applied to excised patches, we studied GABA(A)Rs containing chimeras or exchange mutants between delta and gamma2L subunits to gain insight into the structural bases for fast desensitization and its coupling to deactivation. We demonstrated that the N terminus and two adjacent residues (V233, Y234) in the first transmembrane domain (TM1) of the delta subunit were both required to abolish fast desensitization. Additionally, these residues in TM1 of the gamma2L subunit (Y235, F236) were critical for desensitized states to prolong deactivation after removal of GABA, because mutations resulted in accelerated deactivation despite unaltered desensitization time course. Interestingly, control of desensitization and deactivation was independent of the identity (gamma2L or delta subunit sequence) of TM2, indicating that structures related to the putative channel gate may play a less direct role in desensitization than previously suggested.
Indexed as
Identifiers
11160383PMC6762234What OpenQuestion holds
Registered trials
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.