Abstract
Both in utero exposure to maternal immune activation and cannabis use during adolescence have been associated with increased risk for the development of schizophrenia; however, whether these exposures exert synergistic effects on brain function is not known. In the present study, mild maternal immune activation (MIA) was elicited in mice with prenatal exposure to polyinosinic-polycytidylic acid (poly(I:C)), and ∆9-tetrahydrocannabinol (THC) was provided throughout adolescence in cereal (3 mg/kg/day for 5 days). Neither THC nor MIA pretreatments altered activity in assays used to characterize hyperdopaminergic states in adulthood: amphetamine hyperlocomotion and prepulse inhibition of the acoustic startle reflex. Adolescent THC treatment elicited deficits in spatial memory and enhanced spatial reversal learning in adult female mice in the Morris water maze, while exposure to MIA elicited female-specific deficits in fear extinction learning in adulthood. There were no effects in these assays in adult males, nor were there interactions between THC and MIA in adult females. While doses of poly(I:C) and THC were sufficient to elicit behavioral effects, particularly relating to cognitive performance in females, there was no evidence that adolescent THC exposure synergized with the risk imposed by MIA to worsen behavioral outcomes in adult mice of either sex.
Highlights
Schizophrenia is a psychiatric disease with a multifactorial neurodevelopmental etiology
An enhanced locomotor reaction to low doses of amphetamine is interpreted as a functional imbalance in mesolimbic dopaminergic transmission [11]
But not male, mice exposed to Maternal immune activation (MIA) had enhanced hyperlocomotion following amphetamine
Summary
Schizophrenia is a psychiatric disease with a multifactorial neurodevelopmental etiology. While genetic factors contribute to the risk of schizophrenia, environmental risk factors during critical times of neurodevelopment, the prenatal period and adolescence, contribute to the disease etiology [1]. Maternal immune activation (MIA) is a risk factor for the development of schizophrenia as well as other psychiatric disorders. Prenatal exposure to viral pathogens, such as the influenza virus, is associated with increased incidence of schizophrenia in adulthood. Epidemiological studies demonstrate increased rates of schizophrenia following influenza epidemics [2,3,4,5]. Prenatal exposure to other pathogens has been shown to be associated with schizophrenia [6,7]. The widespread infections of the coronavirus disease 2019 (COVID-19) pandemic increase the need to improve understanding of the effects of MIA on neurodevelopment in offspring
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
