Transient changes in P2X3 but not TRPV1 mRNA expression in rat after prenatal exposure to glucocorticoids

TRPV1 and P2X3 receptors are cation channels known to modulate responses to noxious stimuli. In the nervous system, these receptors are preferentially expressed in the pathways that transmit pain signal from the periphery to the brain. The aim of this study is to determine whether prenatal exposure to glucocorticoids alters the expression of P2X3 and TRPV1 in the dorsal root ganglia (DRG) and spinal cord (SC) during early postnatal development. Time-pregnant rats received daily subcutaneous injection of dexamethasone (100 μg/kg/day) or a vehicle from prenatal days 9 to 20. The DRG and lumbar/sacral SC of the newborn rats were harvested on postnatal days 1, 7, and 42 for a quantitative real-time PCR analysis of messenger RNAs. In the control rats, mRNA level of P2X3 and TRPV1 receptors from DRG remained relatively constant from postnatal days 1 to 42 while those from SC were significantly higher on postnatal day 42 than days 1 and 7. Prenatal treatment with dexamethasone significantly decreased P2X3 receptor mRNA level in the DRG and SC on postnatal day 1. Such an effect was no longer statistically significant on postnatal day 7, and disappeared completely on postnatal day 42. Expression of TRPV 1 was not altered by dexamethasone regardless of anatomical localization or developmental stages. Therefore, prenatal exposure to glucocorticoids leads to a transient inhibition of P2X3 expression in the DRG and SC, suggesting a potential involvement of P2X3 receptors in the unique profile of pain perception in neonates.