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Letter to the Editor   |    
Impairment of Phosphatidylinositol 3-Kinase Signaling in Schizophrenia: State or Trait?
Undine E. Lang, M.D., Ph.D.
Am J Psychiatry 2010;167:719-719. doi:10.1176/appi.ajp.2010.10010103
View Author and Article Information
Berlin, Germany

The author reports no financial relationships with commercial interests.

Accepted March , 2010.

Copyright © American Psychiatric Association

To the Editor: In their article, published in the April 2010 issue of the Journal, Szabolcs Kéri, M.D., Ph.D., D.Sc., et al. (1) showed that neuregulin 1-dependent activation of phosphatidylinositol 3-kinase signaling was impaired in schizophrenia patients, which was connected to P50-evoked response and thereby influenced sensory gating in patients with first-episode schizophrenia. Phosphatidylinositol 3-kinase and phosphoinositide-dependent protein kinase-1 signaling inhibit glycogen synthase kinase-3β. Our workgroup found increased anxiety behavior in phosphoinositide-dependent protein kinase 1 hypomorphic mice (2) and stress-resistant behavior in glycogen synthase kinase-3β knock-in mice, supporting the role of phosphatidylinositol 3-kinase signaling in anxiety and stress (3). However, Dr. Kéri et al. did not examine the influence of neuroleptic treatment on phosphatidylinositol 3-kinase activity. The highly effective atypical antipsychotics olanzapine and clozapine in contrast to haloperidol have been shown to activate the protein kinase B (AKT) glycogen synthase kinase-3β axis (4). These effects might explain heterogenous findings on the P50-evoked response in schizophrenia patients, which seems to normalize after treatment with clozapine and olanzapine but not after typical drugs (5).

Kéri  S;  Beniczky  S;  Kelemen  O:  Suppression of the P50 evoked response and neuregulin 1-induced AKT phosphorylation in first-episode schizophrenia.  Am J Psychiatry 2010; 167:444—450
[CrossRef] | [PubMed]
 
Ackermann  TF;  Hörtnagl  H;  Wolfer  DP;  Colacicco  G;  Sohr  R;  Lang  F;  Hellweg  R;  Lang  UE:  Phosphatidylinositide dependent kinase deficiency increases anxiety and decreases GABA and serotonin abundance in the amygdala.  Cell Physiol Biochem 2008; 22:735—744
[CrossRef] | [PubMed]
 
Ackermann  TF;  Kempe  DS;  Lang  F;  Lang  UE:  Hyperactivity and enhanced curiosity of mice expressing PKB/SGK-resistant glycogen synthase kinase-3 (GSK—3).  Cell Physiol Biochem 2010 (in press)
 
Aubry  JM;  Schwald  M;  Ballmann  E;  Karege  F:  Early effects of mood stabilizers on the Akt/GSK-3beta signaling pathway and on cell survival and proliferation.  Psychopharmacology 2009; 205:419—429
[CrossRef] | [PubMed]
 
Light  GA;  Geyer  MA;  Clementz  BA;  Cadenhead  KS;  Braff  DL:  Normal P50 suppression in schizophrenia patients treated with atypical antipsychotic medications.  Am J Psychiatry 2000; 157:767—771
[CrossRef] | [PubMed]
 
References Container
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References

Kéri  S;  Beniczky  S;  Kelemen  O:  Suppression of the P50 evoked response and neuregulin 1-induced AKT phosphorylation in first-episode schizophrenia.  Am J Psychiatry 2010; 167:444—450
[CrossRef] | [PubMed]
 
Ackermann  TF;  Hörtnagl  H;  Wolfer  DP;  Colacicco  G;  Sohr  R;  Lang  F;  Hellweg  R;  Lang  UE:  Phosphatidylinositide dependent kinase deficiency increases anxiety and decreases GABA and serotonin abundance in the amygdala.  Cell Physiol Biochem 2008; 22:735—744
[CrossRef] | [PubMed]
 
Ackermann  TF;  Kempe  DS;  Lang  F;  Lang  UE:  Hyperactivity and enhanced curiosity of mice expressing PKB/SGK-resistant glycogen synthase kinase-3 (GSK—3).  Cell Physiol Biochem 2010 (in press)
 
Aubry  JM;  Schwald  M;  Ballmann  E;  Karege  F:  Early effects of mood stabilizers on the Akt/GSK-3beta signaling pathway and on cell survival and proliferation.  Psychopharmacology 2009; 205:419—429
[CrossRef] | [PubMed]
 
Light  GA;  Geyer  MA;  Clementz  BA;  Cadenhead  KS;  Braff  DL:  Normal P50 suppression in schizophrenia patients treated with atypical antipsychotic medications.  Am J Psychiatry 2000; 157:767—771
[CrossRef] | [PubMed]
 
References Container
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