Transient changes in P2X3 but not TRPV1 mRNA expression in rat after prenatal exposure to glucocorticoids.
TRPV(1) and P2X(3) 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 P2X(3) and TRPV(1) in the dorsal root ganglia (DRG) and spinal cord (SC) during early postnatal development. Time-pregnant rats received daily subcutaneous injection of dexamethasone (100 microg/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 P2X(3) and TRPV(1) 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 P2X(3) 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 P2X(3) expression in the DRG and SC, suggesting a potential involvement of P2X(3) receptors in the unique profile of pain perception in neonates.
Wang
Heyang
H
Department of Physiology, Second Military Medical University, Shanghai, 200433, China.
Zhou
Mingyue
M
Department of Physiology, Second Military Medical University, Shanghai, 200433, China.
Cong
Binhai
B
Department of Physiology, Second Military Medical University, Shanghai, 200433, China.
He
Ping
P
Department of Physiology, Second Military Medical University, Shanghai, 200433, China.
Xu
Mingjuan
M
Department of Gynaecology and Obstetrics, Changhai Hospital, Shanghai, 200433, China.
Ni
Xin
X
Department of Physiology, Second Military Medical University, Shanghai, 200433, China.
Ma
Bei
B
Department of Physiology, Second Military Medical University, Shanghai, 200433, China. Electronic address: mabei2004@yahoo.com.cn.
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D003907:Dexamethasone / Q000008:administration & dosage / Q000633:toxicity; D005260:Female; D005727:Ganglia, Spinal / Q000187:drug effects / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D005938:Glucocorticoids / Q000008:administration & dosage / Q000633:toxicity*; D007279:Injections, Subcutaneous; D008161:Lumbosacral Region / Q000294:innervation; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018048:Receptors, Purinergic P2 / Q000235:genetics*; D058477:Receptors, Purinergic P2X3; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013116:Spinal Cord / Q000187:drug effects / Q000378:metabolism; D050916:TRPV Cation Channels / Q000235:genetics*
D005938:Glucocorticoids; C546410:P2rx3 protein, rat; D012333:RNA, Messenger; D018048:Receptors, Purinergic P2; D058477:Receptors, Purinergic P2X3; D050916:TRPV Cation Channels; D003907:Dexamethasone