ArticlePsychopharmacology2024
Neurobehavioral protective effects of Japanese sake yeast supplement against chronic stress-induced anxiety and depression-like symptoms in mice: Possible role of central adenosine receptors.
Article in Psychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Lemon Verbena Extract Enhances Sleep Quality and Duration via Modulation of Adenosine A1 and GABAInternational journal of molecular sciences · 2025Article
- Non-pharmacological therapeutic paradigms in stress-induced depression: from novel therapeutic perspective with focus on cell-based strategies.Acta neuropsychiatrica · 2025Review
- Adenosine signaling: a potential therapeutic target for psychogenic erectile dysfunction.American journal of translational research · 2024Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleUsing routine synthetic drugs in the treatment of psychiatric disorders may have some restrictions due to serious side effects and pharmacoresistance. Some natural agents may be promising alternatives in this case. The neuroprotective activity of the neuromodulator adenosine and its receptor, A
objectiveWe aimed to determine the anxiolytic, antidepressant and sedative effects of Japanese sake yeast as the first report.
methodMice were subjected to a one-week stress protocol and concomitantly treated orally with sake yeast at the dose levels of 100, 200 and 300 mg kg
resultsIn all dose regiments, sake yeast significantly improved functions in the EPM and FST. 200 and 300 mg/kg of sake yeast significantly increased sleep duration and reduced sleep latency. Anxiolytic and antidepressant-like activities of sake yeast were maintained by the injection of ZM241385 (15 mg kg
conclusionsWe conclude that oral sake yeast supplement exerts a neurobehavioral protective effect predominantly by activating central A
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