PMID- 20675200
OWN - NLM
STAT- MEDLINE
DCOM- 20110422
LR  - 20131121
IS  - 1528-8447 (Electronic)
IS  - 1526-5900 (Linking)
VI  - 12
IP  - 1
DP  - 2011 Jan
TI  - Progesterone prevents allodynia after experimental spinal cord injury.
PG  - 71-83
LID - 10.1016/j.jpain.2010.04.013 [doi]
AB  - Chronic pain after spinal cord injury represents a therapeutic challenge. 
      Progesterone, a neuroprotective steroid, has been shown to modulate nociceptive 
      thresholds, whereas its effect on neuropathic pain needs to be further explored. 
      In this study, we evaluated whether progesterone could ameliorate pain-associated 
      behaviors in animals subjected to a spinal cord hemisection. The development of 
      mechanical and cold allodynia was assessed in injured male rats treated with 
      daily injections of progesterone or vehicle. The expression of 
      N-methyl-D-aspartate receptor (NMDAR) subunits, protein kinase C gamma (PKCgamma), 
      preprodynorphin (ppD), and kappa opioid receptor (KOR), key players in chronic 
      pain mechanisms, was determined in the dorsal spinal cord. Twenty-eight days 
      after injury, all vehicle-treated animals presented allodynic behaviors and a 
      marked increase in NMDAR subunits, PKCgamma, and ppD mRNA levels, with no changes in 
      KOR mRNA levels. Progesterone prevented the development of mechanical allodynia 
      and reduced the painful responses to cold stimulation. In correlation with the 
      attenuation of pain behaviors, the steroid prevented NMDAR subunits and PKCgamma 
      mRNAs upregulation, did not modify the elevated ppD mRNA levels, but increased 
      KOR expression. In conclusion, progesterone modulates neuropathic pain after 
      spinal cord injury, creating a favorable molecular environment that may decrease 
      spinal nociceptive signaling. PERSPECTIVE: The present study suggests that 
      progesterone administration could represent an interesting strategy to modulate 
      neuropathic pain circuits after spinal cord injury. Further studies are needed to 
      investigate the potential progesterone receptors involved in these actions.
CI  - Copyright (c) 2011 American Pain Society. Published by Elsevier Inc. All rights 
      reserved.
FAU - Coronel, Maria F
AU  - Coronel MF
AD  - Laboratorio de Bioquimica Neuroendocrina, Instituto de Biologia y Medicina 
      Experimental, CONICET, Buenos Aires, Argentina.
FAU - Labombarda, Florencia
AU  - Labombarda F
FAU - Villar, Marcelo J
AU  - Villar MJ
FAU - De Nicola, Alejandro F
AU  - De Nicola AF
FAU - Gonzalez, Susana L
AU  - Gonzalez SL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100802
PL  - United States
TA  - J Pain
JT  - The journal of pain
JID - 100898657
RN  - 0 (NR2A NMDA receptor)
RN  - 0 (NR2B NMDA receptor)
RN  - 0 (Progestins)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Receptors, Opioid, kappa)
RN  - 0 (Tuberculin)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - EC 2.7.1.- (protein kinase C gamma)
RN  - EC 2.7.11.13 (Protein Kinase C)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Functional Laterality
MH  - Gene Expression Regulation/drug effects
MH  - Hyperalgesia/*etiology/*prevention & control
MH  - Male
MH  - Neuralgia/etiology/prevention & control
MH  - Pain Measurement
MH  - Pain Threshold/*drug effects
MH  - Progesterone/*therapeutic use
MH  - Progestins/*therapeutic use
MH  - Protein Kinase C/genetics/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/genetics/metabolism
MH  - Receptors, Opioid, kappa/genetics/metabolism
MH  - Spinal Cord Injuries/*complications
MH  - Tuberculin/genetics/metabolism
EDAT- 2010/08/03 06:00
MHDA- 2011/04/26 06:00
CRDT- 2010/08/03 06:00
PHST- 2010/01/09 00:00 [received]
PHST- 2010/03/18 00:00 [revised]
PHST- 2010/04/29 00:00 [accepted]
PHST- 2010/08/03 06:00 [entrez]
PHST- 2010/08/03 06:00 [pubmed]
PHST- 2011/04/26 06:00 [medline]
AID - S1526-5900(10)00533-X [pii]
AID - 10.1016/j.jpain.2010.04.013 [doi]
PST - ppublish
SO  - J Pain. 2011 Jan;12(1):71-83. doi: 10.1016/j.jpain.2010.04.013. Epub 2010 Aug 2.