Scientific reports, 2017-08, Vol.7 (1), p.7811-12, Article 7811
2017
Details
- Autor(en) / Beteiligte
- Titel
- Isoflurane produces antidepressant effects and induces TrkB signaling in rodents
- Ist Teil von
- Scientific reports, 2017-08, Vol.7 (1), p.7811-12, Article 7811
- Ort / Verlag
- England: Nature Publishing Group
- Erscheinungsjahr
- 2017
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- A brief burst-suppressing isoflurane anesthesia has been shown to rapidly alleviate symptoms of depression in a subset of patients, but the neurobiological basis of these observations remains obscure. We show that a single isoflurane anesthesia produces antidepressant-like behavioural effects in the learned helplessness paradigm and regulates molecular events implicated in the mechanism of action of rapid-acting antidepressant ketamine: activation of brain-derived neurotrophic factor (BDNF) receptor TrkB, facilitation of mammalian target of rapamycin (mTOR) signaling pathway and inhibition of glycogen synthase kinase 3β (GSK3β). Moreover, isoflurane affected neuronal plasticity by facilitating long-term potentiation in the hippocampus. We also found that isoflurane increased activity of the parvalbumin interneurons, and facilitated GABAergic transmission in wild type mice but not in transgenic mice with reduced TrkB expression in parvalbumin interneurons. Our findings strengthen the role of TrkB signaling in the antidepressant responses and encourage further evaluation of isoflurane as a rapid-acting antidepressant devoid of the psychotomimetic effects and abuse potential of ketamine.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 2045-2322eISSN: 2045-2322DOI: 10.1038/s41598-017-08166-9Titel-ID: cdi_doaj_primary_oai_doaj_org_article_9b0a9c01a2904ac9a4a5d9e945138f61
- Format
- –
- Schlagworte
- Anesthesia, Antidepressants, Brain-derived neurotrophic factor, Drug abuse, Glycogen, Glycogen synthase kinase 3, Interneurons, Isoflurane, Ketamine, Kinases, Learned helplessness, Long-term potentiation, Mental depression, Neural plasticity, Parvalbumin, Rapamycin, Rodents, Signal transduction, TOR protein, Transgenic mice, TrkB receptors, γ-Aminobutyric acid