This 2015 French/Italian rodent study found:
“Chronic systemic treatment with carbetocin [unavailable in the US] in PRS [prenatally restraint stressed] rats corrected:
- in social behavior,
- in the HPA response to stress, and
- in the expression of stress-related genes in the hippocampus and amygdala.
These findings disclose a novel function of oxytocin receptors in the hippocampus, and encourage the use of oxytocin receptor agonists in the treatment of stress-related psychiatric disorders in adult life.”
The adult male subjects were:
“PRS rats..the offspring of dams exposed to repeated episodes of restraint stress during pregnancy.
These rats display anxiety- and depressive-like behaviors and show an excessive glucocorticoid response to acute stress, which is indicative of a dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis caused by an impaired hippocampal glucocorticoid negative feedback.
PRS rats show a selective reduction in glutamate release in the ventral hippocampus.”
The researchers cited several other studies they have performed with the PRS phenotype. In the current study:
“Carbetocin treatment had no effect on these behavioral and neuroendocrine parameters in prenatally unstressed (control) rats, with the exception of a reduced expression of the oxytocin receptor gene in the amygdala.
Carbetocin displayed a robust therapeutic activity in PRS rats, but had no effect in unstressed rats, therefore discriminating between physiological and pathological conditions.”
The PRS phenotype showed the ease with which a child can be epigenetically changed – even before they’re born – to be less capable over their entire life. Just stress the pregnant mother-to-be.
http://www.psyneuen-journal.com/article/S0306-4530%2815%2900239-5/abstract “Activation of presynaptic oxytocin receptors enhances glutamate release in the ventral hippocampus of prenatally restraint stressed rats” Thanks to coauthor Dr. Eleonora Gatta for providing the full study.