ArticleMolecular pharmacology2015
Synaptic-type α1β2γ2L GABAA receptors produce large persistent currents in the presence of ambient GABA and anesthetic drugs.
Article in Molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Electrophysiology of ionotropic GABA receptors.Cellular and molecular life sciences : CMLS · 2021Review
- Steady-state activation and modulation of the synaptic-type α1β2γ2L GABAPhysiological reports · 2019Article
- Application of the Co-Agonist Concerted Transition Model to Analysis of GABAA Receptor Properties.Current neuropharmacology · 2019Review
- Comparison of αβδ and αβγ GABAPharmacological research · 2018Review
- Flow characterization and patch clamp dose responses using jet microfluidics in a tubeless microfluidic device.Journal of neuroscience methods · 2017Article
- Comparison of Steroid Modulation of Spontaneous Inhibitory Postsynaptic Currents in Cultured Hippocampal Neurons and Steady-State Single-Channel Currents from Heterologously Expressed α1β2γ2L GABA(A) Receptors.Molecular pharmacology · 2016Article
- Context-Dependent Modulation of GABAAR-Mediated Tonic Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Etomidate uniquely modulates the desensitization of recombinant α1β3δ GABA(A) receptors.Neuroscience · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution.
Funding
Abstract
Synaptic GABAA receptors respond to synaptically released GABA and are considered to be unaffected by the low levels of ambient transmitter in the brain. We show that synaptic-type α1β2γ2L GABAA receptors expressed in HEK293 cells respond with large steady-state currents to combinations of a low concentration (0.5 μM) of GABA and clinically used GABAergic modulators propofol, etomidate, or pentobarbital or the steroid alphaxalone. At a maximally effective concentration of modulator, the current levels at the end of 2-minute applications of drug combinations were >10% of the peak response to saturating GABA. In the absence of modulators, 0.5 μM GABA generated a steady-state response of 1% of the peak response to saturating GABA. The concentration-response curves for enhancement of steady-state currents by propofol, etomidate, pentobarbital, or alphaxalone were at similar or lower drug concentrations compared with concentration-response relationships for enhancement of peak responses. We propose that modulation of tonically activated synaptic-type GABAA receptors contributes to the clinical actions of sedative drugs.
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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.