ArticleJournal of neurophysiology2013
Interaction of anesthetics with neurotransmitter release machinery proteins.
Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Sedative effects of oral pregabalin premedication on intravenous sedation using propofol target-controlled infusion.Journal of anesthesia · 2017Trial
- Disruption of a selective vesicle pool upon retrograde amnesia dissociates memory at presynaptic terminals.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Synapse-Specific Trapping of SNARE Machinery Proteins in the AnesthetizedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Time to Wake Up! The Ongoing Search for General Anesthetic Reversal Agents.Anesthesiology · 2024Article
- Effects of propofol on presynaptic synapsin phosphorylation in the mouse brain in vivo.Brain research · 2024Article
- A primordial target: Mitochondria mediate both primary and collateral anesthetic effects of volatile anesthetics.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Rapamycin Affects the Hippocampal SNARE Complex to Alleviate Cognitive Dysfunction Induced by Surgery in Aged Rats.Brain sciences · 2023Article
- Isoflurane inhibition of endocytosis is an anesthetic mechanism of action.Current biology : CB · 2022Article
- A Common Human Brain-Derived Neurotrophic Factor Polymorphism Leads to Prolonged Depression of Excitatory Synaptic Transmission by Isoflurane in Hippocampal Cultures.Frontiers in molecular neuroscience · 2022Article
- Effects of General Anesthetics on Synaptic Transmission and Plasticity.Current neuropharmacology · 2022Review
- Cell-type-specific imaging of neurotransmission reveals a disrupted excitatory-inhibitory cortical network in isoflurane anaesthesia.EBioMedicine · 2021Article
- Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics.Journal of visualized experiments : JoVE · 2020Article
- Frequency-Dependent Block of Excitatory Neurotransmission by Isoflurane via Dual Presynaptic Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The Effects of General Anesthetics on Synaptic Transmission.Current neuropharmacology · 2020Review
- SNARE Complex-Associated Proteins and Alcohol.Alcoholism, clinical and experimental research · 2020Review
- Selective effects of isoflurane on cortico-cortical feedback afferent responses in murine non-primary neocortex.British journal of anaesthesia · 2019Article
- Neonatal anesthesia impairs synapsin 1 and synaptotagmin 1, two key regulators of synaptic vesicle docking and fusion.Neuroreport · 2019Article
- Isoflurane disrupts excitatory neurotransmitter dynamics via inhibition of mitochondrial complex I.British journal of anaesthesia · 2018Article
- Linear transformation of the encoding mechanism for light intensity underlies the paradoxical enhancement of cortical visual responses by sevoflurane.The Journal of physiology · 2017Article
- Isoflurane inhibits synaptic vesicle exocytosis through reduced Ca2+ influx, not Ca2+-exocytosis coupling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
General anesthetics produce anesthesia by depressing central nervous system activity. Activation of inhibitory GABA(A) receptors plays a central role in the action of many clinically relevant general anesthetics. Even so, there is growing evidence that anesthetics can act at a presynaptic locus to inhibit neurotransmitter release. Our own data identified the neurotransmitter release machinery as a target for anesthetic action. In the present study, we sought to examine the site of anesthetic action more closely. Exocytosis was stimulated by directly elevating the intracellular Ca(2+) concentration at neurotransmitter release sites, thereby bypassing anesthetic effects on channels and receptors, allowing anesthetic effects on the neurotransmitter release machinery to be examined in isolation. Three different PC12 cell lines, which had the expression of different release machinery proteins stably suppressed by RNA interference, were used in these studies. Interestingly, there was still significant neurotransmitter release when these knockdown PC12 cells were stimulated. We have previously shown that etomidate, isoflurane, and propofol all inhibited the neurotransmitter release machinery in wild-type PC12 cells. In the present study, we show that knocking down synaptotagmin I completely prevented etomidate from inhibiting neurotransmitter release. Synaptotagmin I knockdown also diminished the inhibition produced by propofol and isoflurane, but the magnitude of the effect was not as large. Knockdown of SNAP-25 and SNAP-23 expression also changed the ability of these three anesthetics to inhibit neurotransmitter release. Our results suggest that general anesthetics inhibit the neurotransmitter release machinery by interacting with multiple SNARE and SNARE-associated proteins.
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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.