Does nicotine exposure during adolescence modify the course of schizophrenia-like symptoms? Behavioral analysis in a phencyclidine-induced mice model
Autor: | Julyana G. Maia, Alex C. Manhães, Yael Abreu-Villaça, Cláudio C. Filgueiras, Keila A. Semeão, Luciana A. Couto, Ana C. Dutra‐Tavares, Anderson Ribeiro-Carvalho |
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Rok vydání: | 2021 |
Předmět: |
Male
Nicotinic Acetylcholine Receptors Physiology Anti-Addiction Drug Therapy Phencyclidine Social Sciences Biochemistry Open field Nicotine Mice Habits Medicine and Health Sciences Smoking Habits Psychology Public and Occupational Health Prepulse inhibition Multidisciplinary Behavior Animal Animal Behavior Pharmaceutics Animal Models Sensory Gating Nicotine Addiction Chemistry Experimental Organism Systems Schizophrenia Physical Sciences Medicine Female Locomotion Research Article Signal Transduction medicine.drug Neurological Drug Therapy Transmembrane Receptors Substance-Related Disorders NICOTINE EXPOSURE Science Addiction Mouse Models Motor Activity Research and Analysis Methods Alkaloids Model Organisms Drug Therapy Nicotine Replacement Therapy Mental Health and Psychiatry medicine Animals Behavior Biological Locomotion business.industry Chemical Compounds Biology and Life Sciences Proteins Recognition Psychology Cell Biology medicine.disease Nicotine replacement therapy Comorbidity Disease Models Animal Acetylcholine Receptors Animal Studies business Zoology |
Zdroj: | PLoS ONE, Vol 16, Iss 9, p e0257986 (2021) PLoS ONE |
ISSN: | 1932-6203 |
DOI: | 10.1371/journal.pone.0257986 |
Popis: | The first symptoms of schizophrenia (SCHZ) are usually observed during adolescence, a developmental period during which first exposure to psychoactive drugs also occurs. These epidemiological findings point to adolescence as critical for nicotine addiction and SCHZ comorbidity, however it is not clear whether exposure to nicotine during this period has a detrimental impact on the development of SCHZ symptoms since there is a lack of studies that investigate the interactions between these conditions during this period of development. To elucidate the impact of a short course of nicotine exposure across the spectrum of SCHZ-like symptoms, we used a phencyclidine-induced adolescent mice model of SCHZ (2.5mg/Kg, s.c., daily, postnatal day (PN) 38-PN52; 10mg/Kg on PN53), combined with an established model of nicotine minipump infusions (24mg/Kg/day, PN37-44). Behavioral assessment began 4 days after the end of nicotine exposure (PN48) using the following tests: open field to assess the hyperlocomotion phenotype; novel object recognition, a declarative memory task; three-chamber sociability, to verify social interaction and prepulse inhibition, a measure of sensorimotor gating. Phencyclidine exposure evoked deficits in all analyzed behaviors. Nicotine history reduced the magnitude of phencyclidine-evoked hyperlocomotion and impeded the development of locomotor sensitization. It also mitigated the deficient sociability elicited by phencyclidine. In contrast, memory and sensorimotor gating deficits evoked by phencyclidine were neither improved nor worsened by nicotine history. In conclusion, our results show for the first time that nicotine history, restricted to a short period during adolescence, does not worsen SCHZ-like symptoms evoked by a phencyclidine-induced mice model. |
Databáze: | OpenAIRE |
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