Petronijević, Nataša (6506911099)Nataša (6506911099)PetronijevićRadonjić, Nevena V. (23390243000)Nevena V. (23390243000)Radonjić2025-06-122025-06-122016https://doi.org/10.1016/B978-0-12-800212-4.00057-1https://www.scopus.com/inward/record.uri?eid=2-s2.0-84969674432&doi=10.1016%2fB978-0-12-800212-4.00057-1&partnerID=40&md5=be48cda5f842129ee36aeb1e9fbf4c47https://remedy.med.bg.ac.rs/handle/123456789/7698Phencyclidine (PCP), a dissociative anesthetic often abused as a hallucinogen, can induce schizophrenia-like psychosis, including positive and negative symptoms and cognitive dysfunction. PCP is a noncompetitive antagonist of the N-methyl-. d-aspartate receptor (NMDAR). NMDAR hypofunction has been proposed to be a critical component of the pathophysiology of schizophrenia, promoting deficits in gamma-aminobutyric acid (GABA)ergic signaling. Perinatal PCP administration to rodents represents one of the actual animal models of schizophrenia. Here, we explore acute and long-term effects of perinatal PCP administration on the expression of neuregulin-1, a putative risk gene described in schizophrenia. Furthermore, the effects of perinatal PCP treatment on the density of different subclasses of GABAergic cortical interneurons, redox homeostasis, and susceptibility of cortical interneurons to harmful effects of free radicals are discussed. © 2016 Elsevier Inc. All rights reserved.GABAInterneuronsNeuregulin-1PhencyclidineRedox dysregulation