Maternal prenatal stress in rats influences c-fos expression in the spinal cord of the offspring

Previous studies in humans have reported a link between maternal stress and disturbed infant physiological behavior. The objective of our study was to examine in experimental rats how maternal prenatal stress induced by a forced swim test affects offspring afferent spinal responses mediated by stimulation of vaginocervical receptors. The activation of spinal cord neurons showing c-fos expression was examined following vaginocervical mechanical stimulation in adult rats, which were the offspring of dams exposed to gestational stress from E10 until delivery. Vaginocervical stimulation of both prenatal-stressed and non-prenatal-stressed rats induced an increase in immunoreactive protein in the spinal cord ranging from T12 to S1 segmental levels. However, a significantly higher (40%) increase in the expression of Fos-immunoreactive neurons was observed in vaginocervical stimulated prenatally stressed rats than in non-stimulated prenatally stressed ones. This increase was higher in L5–S1 levels than in T12–L4. When the regional distribution was examined, results showed that up to 80% of activated neurons were located in the dorsal horn in both non-stimulated prenatally stressed and stimulated prenatally stressed groups, with a significantly higher density in the latter. Our results demonstrate that maternal prenatal stress can have consequences on vaginocervical responses conveyed to the spinal cord. The increase in Fos labeled neurons in T12–S1 in prenatally stressed rats induced by vaginocervical stimulation suggests the hypersensitivity of the genital tract associated with activation of spinal circuits spanning multiple segments.