Prenatal exposure to tetrahydrocannabinol in cannabis causes spatial memory impairment, especially in male offspring
Long-term hippocampal interneuronopathy drives sex-dimorphic spatial memory impairment induced by prenatal THC exposure
Although exposure to cannabinoids alters many pathways and processes in adult brains, exposure of the immature brains to cannabinoids exerts especially profound deleterious functional consequences. This is because these compounds can interfere with neural cell development, differentiation and connectivity and consequently cause permanent defects to the developing brains. The most prominent active constituent in cannabis plant is tetrahydrocannabinol (THC) because of its high abundance and its high potency to affect the functions of the cannabinoid CB1 receptor (CB1R), a common and important receptor in the brain. THC affects the development of pyramidal neurons and GABAergic interneurons via cannabinoid CB1 receptors (CB1R).
Until recently, the link between THC’s impacts on these two groups of neurons and its induction of behavioral alterations and functional deficits in organisms remained unknown. However, recently, research has revealed that exposure of THC to the embryo leads to alterations in hippocampal oscillations and brain hyperexcitability in the offspring. The oscillations naturally exhibited by the hippocampus are crucial for learning and memory consolidation; thus, changes in these oscillations underlie impaired spatial memory. An abnormally high excitation state compared to inhibition state of the brain results in a higher susceptibility to seizures. Most interestingly, scientists found potential sex differences in these consequences, with male offspring suffering more severe, long-term impacts.