ArticleAnesthesiology2014
General anesthetic isoflurane modulates inositol 1,4,5-trisphosphate receptor calcium channel opening.
Article in Anesthesiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Sevoflurane upregulates neuron death process-related Ddit4 expression by NMDAR in the hippocampus.Aging · 2023Article
- Anesthetics and Cell-Cell Communication: Potential CaInternational journal of molecular sciences · 2022Review
- Nonapoptotic caspases in neural development and in anesthesia-induced neurotoxicity.Trends in neurosciences · 2022Review
- Calcium Ions Aggravate Alzheimer's Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits.Frontiers in molecular neuroscience · 2021Review
- Sevoflurane modulates breast cancer cell survival via modulation of intracellular calcium homeostasis.BMC anesthesiology · 2020Article
- Propofol affects mouse embryonic fibroblast survival and proliferation in vitro via ATG5- and calcium-dependent regulation of autophagy.Acta pharmacologica Sinica · 2020Article
- General Anesthetic-Induced Neurotoxicity in the Immature Brain: Reevaluating the Confounding Factors in the Preclinical Studies.BioMed research international · 2020Review
- Lasting effects of general anesthetics on the brain in the young and elderly: "mixed picture" of neurotoxicity, neuroprotection and cognitive impairment.Journal of anesthesia · 2019Review
- Alzheimer's Disease Presenilin-1 Mutation Sensitizes Neurons to Impaired Autophagy Flux and Propofol Neurotoxicity: Role of Calcium Dysregulation.Journal of Alzheimer's disease : JAD · 2019Article
- Anesthetic effects of isoflurane and the molecular mechanism underlying isoflurane‑inhibited aggressiveness of hepatic carcinoma.Molecular medicine reports · 2018Article
- Protective Effect of Extract ofTranslational neuroscience · 2018Article
- General Anesthetics Regulate Autophagy via Modulating the Inositol 1,4,5-Trisphosphate Receptor: Implications for Dual Effects of Cytoprotection and Cytotoxicity.Scientific reports · 2017Article
- Propofol Affects Neurodegeneration and Neurogenesis by Regulation of Autophagy via Effects on Intracellular Calcium Homeostasis.Anesthesiology · 2017Article
- High Glucose Enhances Isoflurane-Induced Neurotoxicity by Regulating TRPC-Dependent Calcium Influx.Neurochemical research · 2017Article
- Effect of repeated neonatal sevoflurane exposure on the learning, memory and synaptic plasticity at juvenile and adult age.American journal of translational research · 2017Article
- Volatile anaesthetics enhance the metastasis related cellular signalling including CXCR2 of ovarian cancer cells.Oncotarget · 2016Article
- Dantrolene, a treatment for Alzheimer disease?Alzheimer disease and associated disordersReview
- Anesthetic neurotoxicity: Apoptosis and autophagic cell death mediated by calcium dysregulation.Neurotoxicology and teratologyReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 3 countries.
Funding
Abstract
backgroundPharmacological evidence suggests that inhalational general anesthetics induce neurodegeneration in vitro and in vivo through overactivation of inositol trisphosphate receptor (InsP3R) Ca-release channels, but it is not clear whether these effects are due to direct modulation of channel activity by the anesthetics.
methodsUsing single-channel patch clamp electrophysiology, the authors examined the gating of rat recombinant type 3 InsP3R (InsP3R-3) Ca-release channels in isolated nuclei (N = 3 to 15) from chicken lymphocytes modulated by isoflurane at clinically relevant concentrations in the absence and presence of physiological levels of the agonist inositol 1,4,5-trisphosphate (InsP3). The authors also examined the effects of isoflurane on InsP3R-mediated Ca release from the endoplasmic reticulum and changes in intracellular Ca concentration ([Ca]i).
resultsClinically relevant concentrations (approximately 1 minimal alveolar concentration) of the commonly used general anesthetic, isoflurane, activated InsP3R-3 channels with open probability similar to channels activated by 1 µM InsP3 (Po ≈ 0.2). This isoflurane modulation of InsP3R-3 Po depended biphasically on [Ca]i. Combination of isoflurane with subsaturating levels of InsP3 in patch pipettes resulted in at least two-fold augmentations of InsP3R-3 channel Po compared with InsP3 alone. These effects were not noted in the presence of saturating [InsP3]. Application of isoflurane to DT40 cells resulted in a 30% amplification of InsP3R-mediated [Ca]i oscillations, whereas InsP3-induced increase in [Ca]i and cleaved caspase-3 activity were enhanced by approximately 2.5-fold.
conclusionThese results suggest that the InsP3R may be a direct molecular target of isoflurane and plays a role in the mechanisms of anesthetic-mediated pharmacological or neurotoxic effects.
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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.