ArticleIranian journal of medical sciences2016
Effects of Ketamine on Neuronal Spontaneous Excitatory Postsynaptic Currents and Miniature Excitatory Postsynaptic Currents in the Somatosensory Cortex of Rats.
Article in Iranian journal of medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- S-Ketamine Preserves Oxidative Metabolism and Reduces Metabolic Stress During Neuronal Hyperexcitability.International journal of molecular sciences · 2026Article
- Neural Circuit Mechanisms of General Anaesthesia Induction: Current Advances and Future Directions.Current neuropharmacology · 2026Review
- Use of Continuous Ketamine Infusion as an Adjunctive Agent in Young Infants With Refractory and Super Refractory Status Epilepticus: A Case Series.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2023Article
- s-ketamine enhances thalamocortical and corticocortical synaptic transmission in acute murine brain slicesFrontiers in systems neuroscience · 2022Article
- Ketamine attenuates the glutamatergic neurotransmission in the ventral posteromedial nucleus slices of rats.BMC anesthesiology · 2017Article
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
backgroundKetamine is a commonly used intravenous anesthetic which produces dissociation anesthesia, analgesia, and amnesia. The mechanism of ketamine-induced synaptic inhibition in high-level cortical areas is still unknown. We aimed to elucidate the effects of different concentrations of ketamine on the glutamatergic synaptic transmission of the neurons in the primary somatosensory cortex by using the whole-cell patch-clamp method.
methodsSprague-Dawley rats (11-19 postnatal days, n=36) were used to obtain brain slices (300 μM). Spontaneous excitatory postsynaptic currents (data from 40 neurons) were recorded at a command potential of -70 mV in the presence of bicuculline (a competitive antagonist of GABAA receptors, 30 μM) and strychnine (glycine receptor antagonist, 30 μM). Miniature excitatory postsynaptic currents (data from 40 neurons) were also recorded when 1 μM of tetrodotoxin was added into the artificial cerebrospinal fluid. We used GraphPad Prism5for statistical analysis. Significant differences in the mean amplitude and frequency were tested using the Student paired 2-tailed t test. Values of P<0.05 were considered significant.
resultsDifferent concentrations of ketamine inhibited the frequency and amplitude of the spontaneous excitatory postsynaptic currents as well as the amplitude of the miniature excitatory postsynaptic currents in a concentration-dependent manner, but they exerted no significant effect on the frequency of the miniature excitatory postsynaptic currents.
conclusionKetamine inhibited the excitatory synaptic transmission of the neurons in the primary somatosensory cortex. The inhibition may have been mediated by a reduction in the sensitivity of the postsynaptic glutamatergic receptors.
Indexed as
Identifiers
27365548PMC4912645W2420223312What OpenQuestion holds
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.