The American Psychiatric Association (APA) has updated its Privacy Policy and Terms of Use, including with new information specifically addressed to individuals in the European Economic Area. As described in the Privacy Policy and Terms of Use, this website utilizes cookies, including for the purpose of offering an optimal online experience and services tailored to your preferences.

Please read the entire Privacy Policy and Terms of Use. By closing this message, browsing this website, continuing the navigation, or otherwise continuing to use the APA's websites, you confirm that you understand and accept the terms of the Privacy Policy and Terms of Use, including the utilization of cookies.

×

Objective

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.

Method

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-3β system was characterized by the measurement of the phosphorylated AKT to total AKT ratio in peripheral B lymphoblasts.

Results

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.

Conclusion

Decreased neuregulin 1-induced activation of the PI3K/AKT system is associated with impaired sensory gating in first-episode schizophrenia.