P50 gating at acute and post-acute phases of first-episode schizophrenia

Department of Physiology, University of Istanbul, Istanbul Medical Faculty, 34093 Capa-Istanbul, Turkey.
Progress in Neuro-Psychopharmacology and Biological Psychiatry (Impact Factor: 3.69). 11/2008; 32(8):1952-6. DOI: 10.1016/j.pnpbp.2008.09.018
Source: PubMed


Deficit in P50 sensory gating has repeatedly been shown in schizophrenia. In order to determine the contribution of trait and/or state features to P50 gating deficit in schizophrenia we evaluated the P50 gating in patients with first-episode schizophrenia (FES) at acute and post-acute phases. Subject groups comprised 16 patients with FES and 24 healthy controls. Patients were tested at the acute phase of the illness and retested at the post-acute phase when their positive symptoms improved. During the testing at the acute phase five patients were neuroleptic-naive and the others were taking atypical antipsychotics which were started recently in order to control the acute excitation. Patients were receiving risperidone, olanzapine or quetiapine treatment at the post-acute phase. P50 gating was impaired in patients at the acute phase compared to controls. However, at the post-acute phase P50 gating was increased compared to the acute phase, reaching to the gating values of controls. P50 gating improvement might be emerged from atypical antipsychotic medication, although this can only be definitively determined by randomized studies including different antipsychotics.

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    • "Patterson et al8 concluded that their meta-analysis confirms the existence of event-related potential deficits in schizophrenia, with significance similar to the most robust findings reported in neuroimaging and neuropsychology in schizophrenia. Similar conclusions found also several others meta-analytic or detailed review studies which show sensory gating impairments in early stages of schizophrenia that become more prominent in chronic stages of schizophrenia.8,11,13,15,114 Further meta-analytical data by Chang et al115 confirm that the sensory gating deficit in patients with schizophrenia is well documented; nevertheless, certain findings raise doubts about the validity and utility of the S2/S1 ratio as a measure of sensory gating. "
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    ABSTRACT: Diminished suppression of the P50 auditory evoked potential is a widely used sensory gating phenotype in the molecular genetic studies of schizophrenia. The aim of this study was to explore the relationship between this phenotype and neuregulin 1-related intracellular signaling processes. The P50 evoked potential was recorded in 30 first-episode, never-medicated patients with schizophrenia and in 30 healthy comparison volunteers. Neuregulin 1-induced activation of the phosphoinositide 3'-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3beta system was characterized by the measurement of the phosphorylated AKT to total AKT ratio in peripheral B lymphoblasts. Relative to comparison subjects, patients with first-episode schizophrenia displayed diminished P50 suppression and decreased neuregulin 1-induced AKT phosphorylation. There was a significant relationship between P50 suppression and AKT phosphorylation. Decreased neuregulin 1-induced activation of the PI3K/AKT system is associated with impaired sensory gating in first-episode schizophrenia.
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