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Thiamine and benfotiamine improve cognition and ameliorate GSK-3β-associated stress-induced behaviours in mice

Thiamine (vitamin B1) deficiency in the brain has been implicated in the development of dementia and symptoms of depression. Indirect evidence suggests that thiamine may contribute to these pathologies by controlling the activities of glycogen synthase kinase (GSK)-3β. While decreased GSK-3β activit...

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Published in:Progress in neuro-psychopharmacology & biological psychiatry 2017-04, Vol.75, p.148-156
Main Authors: Markova, Nataliia, Bazhenova, Nataliia, Anthony, Daniel C., Vignisse, Julie, Svistunov, Andrey, Lesch, Klaus-Peter, Bettendorff, Lucien, Strekalova, Tatyana
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description Thiamine (vitamin B1) deficiency in the brain has been implicated in the development of dementia and symptoms of depression. Indirect evidence suggests that thiamine may contribute to these pathologies by controlling the activities of glycogen synthase kinase (GSK)-3β. While decreased GSK-3β activity appears to impair memory, increased GSK-3β activity is associated with the distressed/depressed state. However, hitherto direct evidence for the effects of thiamine on GSK-3β function has not been reported. Here, we administered thiamine or, the more bioavailable precursor, benfotiamine at 200mg/kg/day for 2weeks to C57BL/6J mice, to determine whether treatment might affect behaviours that are known to be sensitive to GSK-3β activity and whether such administration impacts on GSK-3β expression within the brain. The mice were tested in models of contextual conditioning and extinction, a 5-day rat exposure stress test, and a modified swim test with repeated testing. The tricyclic antidepressant imipramine (7.5mg/kg/day), was administered as a positive control for the effects of thiamine or benfotiamine. As for imipramine, both compounds inhibited the upregulation of GSK-3β induced by predator stress or repeated swimming, and reduced floating scores and the predator stress-induced behavioural changes in anxiety and exploration. Coincident, thiamine and benfotiamine improved learning and extinction of contextual fear, and the acquisition of the step-down avoidance task. Our data indicate that thiamine and benfotiamine have antidepressant/anti-stress effects in naïve animals that are associated with reduced GSK-3β expression and conditioning of adverse memories. Thus thiamine and benfotiamine may modulate GSK-3β functions in a manner that is dependent on whether the contextual conditioning is adaptive or maladaptive. •Thiamine and benfotiamine generate antistress and antidepressant-like effects in mice.•Both molecules prevent brain activation of GSK3-β in a model of depression.•Each also prevent stress-induced increases in anxiety and GSK3-β expression.•Thiamine and benfotiamine enhance contextual memory and extinction in naïve mice.•The effects on stress and learning are likely to be mediated via distinct mechanisms.
doi_str_mv 10.1016/j.pnpbp.2016.11.001
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source ScienceDirect Journals
subjects Animal models
Animals
Avoidance Learning - drug effects
Benfotiamine
Brain - drug effects
Brain - enzymology
Cognition Disorders - drug therapy
Cognition Disorders - etiology
Cognition Disorders - pathology
Conditioning (Psychology) - drug effects
Depression
Disease Models, Animal
Extinction, Psychological - drug effects
Fear - drug effects
Gene Expression Regulation - drug effects
Glycogen Synthase Kinase 3 beta - genetics
Glycogen Synthase Kinase 3 beta - metabolism
Glycogene-synthase-kinase-3-beta (GSK-3β)
Male
Mice
Mice, Inbred C57BL
Plasticity
RNA, Messenger - metabolism
Stress, Psychological - complications
Stress, Psychological - drug therapy
Stress, Psychological - metabolism
Swimming - psychology
Thiamine
Thiamine - analogs & derivatives
Thiamine - pharmacology
Thiamine - therapeutic use
Time Factors
Vitamin B Complex - therapeutic use
title Thiamine and benfotiamine improve cognition and ameliorate GSK-3β-associated stress-induced behaviours in mice
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