Halothane modulates NMDA and non-NMDA excitatory synaptic transmission in rat cortical neurons

Kitamura, Akira; Satoh, Ryoichi; Nagano, Tomoo; Matsuda, Hiroyuki; Shimizu, Tôru; Sakamoto, Atsuhiro; Ogawa, Ryo

doi:10.1007/s00540-004-0285-x

Cited by 4 publications

(5 citation statements)

References 28 publications

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“…In recent years, many in vitro studies have shown that the mechanism of anesthesia may involve cell membranes, multiple receptors, ion channels, and neurotransmitters [10][11][12]. The N-methyl-D-aspartate (NMDA) receptor is an important excitatory amino acid receptor in the central nervous system.…”

Section: Introductionmentioning

confidence: 99%

GABAA Receptor/STEP61 Signaling Pathway May Be Involved in Emulsified Isoflurane Anesthesia in Rats

Zhao

Chang

Cheng

et al. 2020

IJMS

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(1) Background: Emulsified isoflurane (EISO) is a type of intravenous anesthetic. How emulsified isoflurane works in the brain is still unclear. The aim of this study was to explore whether epigenetic mechanisms affect anesthesia and to evaluate the anesthetic effects of emulsified isoflurane in rats. (2) Methods: Rats were randomly divided into four groups (n = 8/group): The tail vein was injected with normal saline 0.1 mL·kg−1·min−1 for the control (Con) group, with intralipid for the fat emulsion (FE) group, with EISO at 60 mg·kg−1·min−1 for the high-concentration (HD) group, and 45 mg·kg−1·min−1 for the low-concentration (LD) group. The consciousness state, motor function of limbs, and response to nociceptive stimulus were observed after drug administration. (3) Results: Using real-time polymerase chain reaction (PCR) to assess the promoter methylation of ion channel proteins in the cerebral cortex of rats anesthetized by EISO, we demonstrated that the change in the promoters’ methylation of the coding genes for gamma-aminobutyric acid A receptor α1 subunit (GABAAα1), N-methyl-D-aspartate receptor subunit 1 (NMDAR1), and mu opioid receptor 1 (OPRM1) was accompanied by the change in messenger ribonucleic acid (mRNA) and protein expression by these genes. (4) Conclusion: These data suggest that the epigenetic factors’ modulation might offer a novel approach to explore the anesthetic mechanism of EISO.

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Section: Introductionmentioning

confidence: 99%

GABAA Receptor/STEP61 Signaling Pathway May Be Involved in Emulsified Isoflurane Anesthesia in Rats

Zhao

Chang

Cheng

et al. 2020

IJMS

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“…This could represent a higher baseline sympathetic tone. With the interplay of disease and anesthesia on the NMDA receptor, potential exists for the exacerbation of neurologic symptoms or paroxysmal sympathetic hyperreactivity (PSH) 5–8 . None of our patients experienced arrhythmias nor hemodynamic lability while under anesthesia.…”

Section: Discussionmentioning

confidence: 89%

“…The NMDA receptor is also a common target for anesthetic agents. Patients with anti‐NMDA receptor encephalitis could potentially have unique anesthetic consequences 5–8 . The anesthetic implications of this disease process are unknown, especially for pediatric patients.…”

Section: Introductionmentioning

confidence: 99%

Anesthesia for pediatric patients with anti‐NMDA receptor encephalitis: A retrospective case series

Bell

Friedman

Matar

et al. 2021

Pediatric Anesthesia

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Introduction Anti‐N‐methyl‐D‐aspartate receptor encephalitis is caused by auto‐antibodies that target the N‐methyl‐D‐aspartate receptor. Autonomic instability is a hallmark of the disease. The objective of this case series is to examine how anesthesia affects pediatric patients with this disease. Methods We performed a retrospective chart review of 28 records in 17 patients who underwent anesthesia. Our primary outcomes were hemodynamic changes during the perioperative period. Heart rate, systolic and diastolic blood pressures, respiratory rate, and oxygen saturation comprise our endpoints. A subgroup of patients, who underwent imaging with anesthesia, was then compared to controls. Results In anti‐N‐methyl‐D‐aspartate receptor encephalitis cases, there were significant percent changes from baseline in heart rate; median = −14.3%, 95% CI (−19.3, −9.0), p < .01 at 30 min and −15.7%, (−21.1, −9.8), p < .01 at 60 min; in systolic blood pressure, −19.4%, (−23.7, −14.8) at 30 min, p < .01, and −14.8%, (−19.7, −9.5) at 60 min, p < .01; in diastolic blood pressure, −41.9%, (−46.9, −36.3), p < .01 at 30 min, and −37.5%, (−43.4, −30.9), p < .01 at 60 min. When compared to controls, there were no significant differences between the two groups across time of anesthesia (baseline to 60 min) in heart rate (p = .24), systolic blood pressure (p = .30), and diastolic blood pressure (p = .11). No patients experienced hemodynamic lability under anesthesia. One patient, with severe symptoms, died within 24 h of anesthesia. Conclusion Although pediatric patients with anti‐N‐methyl‐D‐aspartate receptor encephalitis experienced vital sign changes with anesthesia, they were not clinically significant and they behaved similarly to controls. Disease severity may be a risk factor for perioperative complications.

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“…The mechanisms of action of halogenated agents are complex and not fully understood. Isoflurane and halothane are known to enhance GABA A synaptic inhibition (Antkowiak 1999), and to block NMDA receptors (Ming et al 2002, Kitamura et al 2005). These mechanisms are shared by drugs that had no effect in any of the cases.…”

Section: Methodsmentioning

confidence: 99%

Stimulus‐sensitive burst‐spiking in burst‐suppression in children: implications for management of refractory status epilepticus

Dan,

Boyd

2006

Epileptic Disorders

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Status epilepticus refractory to sequential trials of multiple medication is a rare but significant problem in children. We describe stimulus sensitivity arising during the treatment of convulsive status epilepticus in children (stimulus‐sensitive burst‐spiking in burst‐suppression). We reviewed retrospectively clinical and EEG features in six children (three months to ten years), with status epilepticus requiring intensive care, in whom tactile, auditory and visual stimulation induced myoclonic jerks and bursts of EEG spikes. Sensitivity was not present at onset, but appeared after 24 hours as myoclonic jerks of the eyes, face and limbs, irrespective of the modality and site of stimulation. These were associated with burst‐suppression in the EEG, the induced spiking forming the burst component. Various antiepileptic drugs, including GABAergic and NMDA blockers had no effect, but halogenated agents (used in two patients) abolished the sensitivity. Two children died, but the remainder returned to their previous clinical state. We conclude that stimulus sensitivity may appear in the context of refractory status epilepticus treated with high‐dose barbiturates. Outcome may be more favorable than previously reported in adults, mostly in the context of post‐anoxic or toxic coma. Evaluation of ventilated children in status epilepticus should include electroclinical assessment using sensory stimulation. If present, the drug regime should be reviewed and halogenated agents considered.

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Halothane modulates NMDA and non-NMDA excitatory synaptic transmission in rat cortical neurons

Abstract: These results show that halothane causes decrease of excitatory synaptic activity, with NMDA EPSCs being more sensitive than non-NMDA EPSCs.

Cited by 4 publications

References 28 publications

GABAA Receptor/STEP61 Signaling Pathway May Be Involved in Emulsified Isoflurane Anesthesia in Rats

GABAA Receptor/STEP61 Signaling Pathway May Be Involved in Emulsified Isoflurane Anesthesia in Rats

Anesthesia for pediatric patients with anti‐NMDA receptor encephalitis: A retrospective case series

Stimulus‐sensitive burst‐spiking in burst‐suppression in children: implications for management of refractory status epilepticus

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