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Chronic Antipsychotic Treatment Modulates Aromatase (CYP19A1) Expression in the Male Rat Brain

Authors
  • Bogus, Katarzyna1
  • Pałasz, Artur1
  • Suszka-Świtek, Aleksandra1
  • Worthington, John J.2
  • Krzystanek, Marek3
  • Wiaderkiewicz, Ryszard1
  • 1 Medical University of Silesia, Department of Histology, School of Medicine in Katowice, ul. Medyków Street 18, Katowice, 40-752, Poland , Katowice (Poland)
  • 2 Lancaster University, Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster, LA1 4YQ, UK , Lancaster (United Kingdom)
  • 3 Medical University of Silesia, Department and Clinic Psychiatric Rehabilitation, School of Medicine in Katowice, ul. Ziolowa 45/47, Katowice, 40-635, Poland , Katowice (Poland)
Type
Published Article
Journal
Journal of Molecular Neuroscience
Publisher
Springer-Verlag
Publication Date
Apr 09, 2019
Volume
68
Issue
2
Pages
311–317
Identifiers
DOI: 10.1007/s12031-019-01307-x
Source
Springer Nature
Keywords
License
Green

Abstract

Antipsychotic drugs, known as the antagonists of dopaminergic receptors, may also affect a large spectrum of other molecular signaling pathways in the brain. Despite the numerous ongoing studies on neurosteroid action and regulation, there are no reports regarding the influence of extended treatment with typical and atypical neuroleptics on brain aromatase (CYP19A1) expression. In the present study, we assessed for the first time aromatase mRNA and protein levels in the brain of rats chronically (28 days) treated with olanzapine, clozapine, and haloperidol using quantitative real-time PCR, end-point RT-PCR, and Western blotting. Both clozapine and haloperidol, but not olanzapine treatment, led to an increase of aromatase mRNA expression in the rat brain. On the other hand, aromatase protein level remained unchanged after drug administration. These results cast a new light on the pharmacology of examined antipsychotics and contribute to a better understanding of the mechanisms responsible for their action. The present report also underlines the complex nature of potential interactions between neuroleptic pharmacological effects and physiology of brain neurosteroid pathways.

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