Males exposed to cannabinoids while in the uterus were less sociable than normal animals, and spent less time interacting with others.
The study, conducted over rats, revealed that males exposed to cannabinoids while in the uterus were less sociable than normal animals, and spent less time interacting with others.
Their sniffing and playing behaviours were impaired, while the number of attacks among males remained unchanged.
In addition, the researchers saw that the exposed males had a heightened excitability of pyramidal neurons in the prefrontal cortex. However, none of these effects were seen in females.
"As cannabinoids can cross the placenta, they may interfere with foetal endocannabinoid signalling during neurodevelopment, which is involved in regulating a variety of processes such as pregnancy, appetite, pain sensation, and mediating the pharmacological effects of cannabis," said Olivier Manzoni, Research Director from the French National Institute of Health and Medical Research (INSERM) in Paris.
"This could in turn lead to some serious long-term deficits," Manzoni added.
For the study, published in eLife, the team examined how prenatal cannabinoid exposure influences the synaptic and behavioural functions of the medial prefrontal cortex -- a brain region often implicated in neuropsychiatric disorders -- in adult male and female rats.
While social interaction was specifically impaired in males, locomotion, anxiety and cognition remained unaffected in both sexes, suggesting discrete and sex-specific behavioural consequences of cannabinoid exposure during adulthood, the researchers noted.
The results also revealed that the effects could be because of mGlu5 gene, which was reduced in the exposed males' prefrontal cortex.
Amplifying mGlu5 signalling could normalise the synaptic and behavioural deficits induced by prenatal exposure to cannabinoids partly by activating the cannabinoid type 1 receptor (CB1R).
Similarly, enhancing levels of anandamide (a type of endocannabinoid) in exposed males helped to restore their social deficits via CB1R.
The findings point towards a potential pharmacological strategy to help reverse social deficits in humans, the researchers stated.