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Looking Beyond the Role of Glycogen Synthase Kinase-3 Genetic Expression on Electroretinogram Response: What About Lithium?

  • Joëlle Lavoie
    Affiliations
    Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland

    Centre de recherche de l’Institut Universitaire en Santé Mentale de Québec, Quebec City, Quebec, Canada
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  • Marc Hébert
    Affiliations
    Centre de recherche de l’Institut Universitaire en Santé Mentale de Québec, Quebec City, Quebec, Canada

    Ophthalmology, Otorhinolaryngology and Cervico-Facial Surgery
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  • Jean-Martin Beaulieu
    Correspondence
    Address correspondence to Jean-Martin Beaulieu
    Affiliations
    Centre de recherche de l’Institut Universitaire en Santé Mentale de Québec, Quebec City, Quebec, Canada

    Psychiatry and Neuroscience, Faculty of Medicine, Université Laval, Quebec City, Quebec, Canada
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      We read with great interest the excellent commentary by Chen et al. (
      • Chen G.
      • Henter I.D.
      • Manji H.K.
      Looking ahead: Electroretinogram anomalies, glycogen synthase kinase-3, and biomarkers for neuropsychiatric disorders.
      ) about our two recent publications in Biological Psychiatry documenting the implication of central monoamines neurotransmission (
      • Lavoie J.
      • Illiano P.
      • Sotnikova T.D.
      • Gainetdinov R.R.
      • Beaulieu J.M.
      • Hébert M.
      The electroretinogram as a biomarker of central dopamine and serotonin: Potential relevance to psychiatric disorders.
      ) and glycogen synthase kinase-3 (GSK3) activity (
      • Lavoie J.
      • Hébert M.
      • Beaulieu J.M.
      Glycogen synthase kinase-3 overexpression replicates the electroretinogram anomalies of offspring at high genetic risk for schizophrenia and bipolar disorder.
      ) on electroretinogram (ERG) response profile. In particular, the authors underscored the contribution of GSK3 as a potential risk factor for psychiatric illnesses such as schizophrenia and mood disorders. It has been found that GSK3 acts as a major component of several molecular pathways and is involved in various cell functions (
      • Chen G.
      • Henter I.D.
      • Manji H.K.
      Looking ahead: Electroretinogram anomalies, glycogen synthase kinase-3, and biomarkers for neuropsychiatric disorders.
      ,
      • Li X.
      • Jope R.S.
      Is glycogen synthase kinase-3 a central modulator in mood regulation?.
      ). Numerous genetic and post-mortem brain studies have reported an association between GSK3 expression and psychiatric illnesses (
      • Lavoie J.
      • Hébert M.
      • Beaulieu J.M.
      Glycogen synthase kinase-3 overexpression replicates the electroretinogram anomalies of offspring at high genetic risk for schizophrenia and bipolar disorder.
      ). Furthermore, the Akt-GSK3 signaling cascade is modulated by several pharmacologic agents used for the management of psychiatric diseases, such as the mood stabilizer lithium, which inhibits GSK3 both directly and indirectly (
      • Klein P.S.
      • Melton D.A.
      A molecular mechanism for the effect of lithium on development.
      ,
      • Beaulieu J.M.
      • Marion S.
      • Rodriguiz R.M.
      • Medvedev I.O.
      • Sotnikova T.D.
      • Ghisi V.
      • et al.
      A β-arrestin 2 signaling complex mediates lithium action of behavior.
      ).
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