Background: Maternal stress has been linked with many adverse perinatal outcomes, particularly effects on neurodevelopment and behaviour with male children showing an increased risk for hyperactivity and attention disorders¹ . We have shown that late gestational prenatal stress results in reductions in myelination and reactive astrocyte expression only in male fetuses² . This study aimed to assess if these reductions persisted into adolescence and further to determine any correlation between salivary cortisol levels in offspring and markers of brain development at the time of post mortem.

Method: Stress was induced in pregnant guinea pigs by exposure to strobe light for 2h/day at 50,55, 60 and 65days (term 70days). Neonatal brains were collected 21 days after birth (adolescence) and stained by immunohistochemistry for mature oligodendrocytes (myelin basic protein, MBP) and reactive astrocytes (glial fibrillary acidic protein, GFAP). Saliva was collected immediately prior to tissue collection to measure cortisol levels via ELISA.

Results:  Male adolescents (males n=5) exposed to late gestational prenatal stress show reduced (p<0.01) expression of MBP and GFAP in the hippocampus and subcortical white matter at 21 days of age compared to controls (males n=8, females n=5). There was no effect of prenatal stress exposure on female adolescents (females n=6). Salivary cortisol levels at the time of post mortem were not affected by prenatal stress exposure, nor was there a correlation between cortisol levels and MBP or GFAP expression.

Conclusions: These findings indicate that prenatal stress induced disruptions in fetal brain development do indeed persist to adolescence in males, with no effect of prenatal stress exposure on females. Salivary cortisol levels are not correlated with expression of MBP or GFAP at adolescence. These data need to be considered when assessing outcomes for affected children as male behavioural abnormalities may be linked to deficits in myelination or astrocyte activation.