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
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