ArticleBritish journal of pharmacology2007
Reduced inhibition of cortical glutamate and GABA release by halothane in mice lacking the K+ channel, TREK-1.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- TREK-1 and epilepsy: regulating the balance of KBehavioral and brain functions : BBF · 2025Review
- Interactions between Glycine and Glutamate through Activation of Their Transporters in Hippocampal Nerve Terminals.Biomedicines · 2023Article
- TREK-1 Null Impairs Neuronal Excitability, Synaptic Plasticity, and Cognitive Function.Molecular neurobiology · 2020Article
- Potentiation of Schaffer-Collateral CA1 Synaptic Transmission by eEF2K and p38 MAPK Mediated Mechanisms.Frontiers in cellular neuroscience · 2016Article
- Two-pore domain potassium channels enable action potential generation in the absence of voltage-gated potassium channels.Pflugers Archiv : European journal of physiology · 2015Review
- Two-pore domain potassium channels in the adrenal cortex.Pflugers Archiv : European journal of physiology · 2015Review
- Activation of K(2)P channel-TREK1 mediates the neuroprotection induced by sevoflurane preconditioning.British journal of anaesthesia · 2014Article
- Interaction of anesthetics with neurotransmitter release machinery proteins.Journal of neurophysiology · 2013Article
- Regional differences in the effects of isoflurane on neurotransmitter release.Neuropharmacology · 2011Article
- Anaesthetic mechanisms: update on the challenge of unravelling the mystery of anaesthesia.European journal of anaesthesiology · 2009Review
- Extracellular acidification exerts opposite actions on TREK1 and TREK2 potassium channels via a single conserved histidine residue.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Isoflurane inhibits the neurotransmitter release machinery.Journal of neurophysiology · 2009Article
- Two-pore potassium channels in the cardiovascular system.European biophysics journal : EBJ · 2009Review
- Nicotinic receptor-evoked hippocampal norepinephrine release is highly sensitive to inhibition by isoflurane.British journal of anaesthesia · 2009Article
- Mtap2 is a constituent of the protein network that regulates twik-related K+ channel expression and trafficking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeDeletion of TREK-1, a two-pore domain K(+) channel (K(2P)) activated by volatile anaesthetics, reduces volatile anaesthetic potency in mice, consistent with a role for TREK-1 as an anaesthetic target. We used TREK-1 knockout mice to examine the presynaptic function of TREK-1 in transmitter release and its role in the selective inhibition of glutamate vs GABA release by volatile anaesthetics. EXPERIMENTAL APPROACH: The effects of halothane on 4-aminopyridine-evoked and basal [(3)H]glutamate and [(14)C]GABA release from cerebrocortical nerve terminals isolated from TREK-1 knockout (KO) and littermate wild-type (WT) mice were compared. TREK-1 was quantified by immunoblotting of nerve terminal preparations. KEY
resultsDeletion of TREK-1 significantly reduced the potency of halothane inhibition of 4-aminopyridine-evoked release of both glutamate and GABA without affecting control evoked release or the selective inhibition of glutamate vs GABA release. TREK-1 deletion also reduced halothane inhibition of basal glutamate release, but did not affect basal GABA release. CONCLUSIONS AND IMPLICATIONS: The reduced sensitivity of glutamate and GABA release to inhibition by halothane in TREK-1 KO nerve terminals correlates with the reduced anaesthetic potency of halothane in TREK-1 KO mice observed in vivo. A presynaptic role for TREK-1 was supported by the enrichment of TREK-1 in isolated nerve terminals determined by immunoblotting. This study represents the first evidence for a link between an anaesthetic-sensitive 2-pore domain K(+) channel and presynaptic function, and provides further support for presynaptic mechanisms in determining volatile anaesthetic action.
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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.