ArticleInternational journal of molecular sciences2021
Ketamine Produces a Long-Lasting Enhancement of CA1 Neuron Excitability.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- S-Ketamine Preserves Oxidative Metabolism and Reduces Metabolic Stress During Neuronal Hyperexcitability.International journal of molecular sciences · 2026Article
- Research Progress on the Mechanism of Ketamine in Neuropathic Pain Comorbid Depression.Neuropsychiatric disease and treatment · 2025Review
- Ketamine induced synaptic plasticity operates independently of long-term potentiation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Divergent Effects of Ketamine and the Serotoninergic Psychedelic 2,5-Dimethoxy-4-Iodoamphetamine on Hippocampal Plasticity and Metaplasticity.Psychedelic medicine (New Rochelle, N.Y.) · 2024Article
- New perspective on sustained antidepressant effect: focus on neurexins regulating synaptic plasticity.Cell death discovery · 2024Review
- Sex differences in single neuron function and proteomics profiles examined by patch-clamp and mass spectrometry in the locus coeruleus of the adult mouse.Acta physiologica (Oxford, England) · 2024Article
- Ketamine evoked disruption of entorhinal and hippocampal spatial maps.Nature communications · 2023Article
- Article
- Ketamine and the Disinhibition Hypothesis: Neurotrophic Factor-Mediated Treatment of Depression.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Ketamine evoked disruption of entorhinal and hippocampal spatial maps.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ketamine is a clinical anesthetic and antidepressant. Although ketamine is a known NMDA receptor antagonist, the mechanisms contributing to antidepression are unclear. This present study examined the loci and duration of ketamine's actions, and the involvement of NMDA receptors. Local field potentials were recorded from the CA1 region of mouse hippocampal slices. Ketamine was tested at antidepressant and anesthetic concentrations. Effects of NMDA receptor antagonists APV and MK-801, GABA receptor antagonist bicuculline, and a potassium channel blocker TEA were also studied. Ketamine decreased population spike amplitudes during application, but a long-lasting increase in amplitudes was seen during washout. Bicuculline reversed the acute effects of ketamine, but the washout increase was not altered. This long-term increase was statistically significant, sustained for >2 h, and involved postsynaptic mechanisms. A similar effect was produced by MK-801, but was only partially evident with APV, demonstrating the importance of the NMDA receptor ion channel block. TEA also produced a lasting excitability increase, indicating a possible involvement of potassium channel block. This is this first report of a long-lasting increase in excitability following ketamine exposure. These results support a growing literature that increased GABA inhibition contributes to ketamine anesthesia, while increased excitatory transmission contributes to its antidepressant effects.
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