Mechanisms underlying cognitive impairment induced by prenatal cannabinoid exposure: a literature review

Human and animal studies have revealed that prenatal cannabinoid exposure alters fetal brain development and leads to persistent impairment in the cognitive function of offspring. However, the mechanism underlying the effect of prenatal cannabinoid exposure on cognitive function in offspring is still not fully understood. Therefore, the goal of this literature review is to discuss the published studies on the mechanisms underlying the effects of prenatal cannabinoid exposure on cognitive impairment. The articles used in this prenatal cannabinoid exposure review were retrieved by electronic search of the Medline database for literature describing human and animal models of prenatal cannabinoid exposure from 2006 to 2022. The findings from the studies reviewed revealed that the cognitive impairment associated with prenatal cannabinoid exposure is caused by alterations in the expression and function of endocannabinoid receptor 1 (CB1R), decreased glutamate transmission, reduced neurogenesis, alterations in protein kinase B (PKB/Akt) and extracellular signal‑regulated kinase 1 and 2 (ERK1/2) activity, and increased mitochondrial function in the hippocampus, cortex, and cerebellum. This review briefly touches upon the currently available measurement and prevention methods and their limitations.