Abstract

Clozapine is an antipsychotic that produces serious withdrawal effects in schizophrenic patients. Olfactory deficits are well known as part of negative symptoms, but it is not known whether antipsychotic use and/or withdrawal are implicated. Then, we tested clozapine withdrawal in association with two widely used schizophrenia models: Neonatal immune challenge by Polycitidilic-polyinosinic acid (polyI:C) and ketamine. PolyI:C (or saline) was injected subcutaneously in neonatal period, dose of 5 mg/kg from 2 to 6 Post Natal Days, and ketamine or saline at the dose 25mg/kg intraperitoneally (i.p.), daily for 7 days from 53 to 60 post natal day. Clozapine 10mg/kg (or saline) was administered i.p. from 46 to 60 post natal day. Olfactory discrimination test (sensorial and cognitive deficit) was performed at 61 post natal day, 24h after the last injections. The association of PolyI:C, ketamine and clozapine disrupted Olfactory Discrimination, equating time in familiar and non-familiar compartments. PolyI:C plus ketamine increased crossings between compartments. It was produced, for the first time, an olfactory deficit induced by clozapine withdrawal in Wistar rats subjected to schizophrenia animal models.

Highlights

  • Clozapine is an antipsychotic that produces serious withdrawal effects in schizophrenic patients (Wadekar and Syed 2010, Yeh et al 2004)

  • The present study aims, to verify the role of olfactory deficit as a symptom of clozapine withdrawal in SZ, using two well established SZ models: (Hida et al 2014): neonatal immune challenge with polyinosinic acid (polyI):C

  • Post hoc test revealed that the PolyI:C+ketamine+saline group had increased number of crossings during the task

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Summary

Introduction

Clozapine is an antipsychotic that produces serious withdrawal effects in schizophrenic patients (Wadekar and Syed 2010, Yeh et al 2004). Olfactory deficits are well known in schizophrenic patients, but it is unclear whether such deficits are due to the condition itself, or a side effect of long term antipsychotic use (Ansoleaga et al 2015, Kiparizoska and Ikuta 2017). (Pearce 2001) and N-methyl-D-aspartate receptor hypofunction by subanesthetic doses of ketamine (Zugno et al 2016)

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