PMID- 17084039
OWN - NLM
STAT- MEDLINE
DCOM- 20070315
LR  - 20131121
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 144
IP  - 1
DP  - 2007 Jan 5
TI  - Activation of protein kinase B/Akt in the periphery contributes to pain behavior 
      induced by capsaicin in rats.
PG  - 286-94
AB  - Protein kinase B (PKB/Akt) is a member of the second-messenger regulated 
      subfamily of protein kinases. It is implicated in signaling downstream of growth 
      factors, insulin receptor tyrosine kinases and phosphoinositide 3-kinase (PI3K). 
      Current studies indicate that nerve growth factor (NGF), brain-derived 
      neurotrophic factor (BDNF) and PI3K help mediate inflammatory hyperalgesia. 
      However, little is known about the role of PKB/Akt in the nociceptive system. In 
      this study, we investigated whether PKB/Akt in primary sensory neurons is 
      activated after noxious stimulation and contributes to pain behavior induced in 
      rats by capsaicin. We demonstrated that phospho-PKB/Akt (p-PKB/Akt) is increased 
      in dorsal root ganglia (DRG) at 5 min after intradermal injection of capsaicin. 
      p-PKB/Akt is distributed predominantly in small- and medium-sized DRG cells. 
      After capsaicin injection, p-PKB/Akt (473) is colocalized with isotectin-B4 
      (IB4), tyrosine kinase A (TrkA), and calcitonin gene-related peptide (CGRP). 
      Furthermore, most transient receptor potential vanilloid type 1 (TRPV1) positive 
      DRG neurons double label for p-PKB/Akt. Behavioral experiments show that 
      intradermal injection of a PI3K (upstream of PKB/Akt) inhibitor, wortmannin, 
      dose-dependently inhibits the changes in exploratory behavior evoked by capsaicin 
      injection. The PKB/Akt inhibitor, Akt inhibitor IV, has the same effect. The 
      results suggest that the PKB/Akt signaling pathway in the periphery is activated 
      by noxious stimulation and contributes to pain behavior.
FAU - Sun, R
AU  - Sun R
AD  - Department of Neuroscience and Cell Biology, The University of Texas Medical 
      Branch, 301 University Blvd, Galveston, TX 77555-1069, USA.
FAU - Yan, J
AU  - Yan J
FAU - Willis, W D
AU  - Willis WD
LA  - eng
GR  - NS09743/NS/NINDS NIH HHS/United States
GR  - NS11255/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20061102
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Nerve Tissue Proteins)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - S07O44R1ZM (Capsaicin)
SB  - IM
MH  - Animals
MH  - Behavior, Animal/*drug effects
MH  - Blotting, Western
MH  - Capsaicin/*pharmacology
MH  - Enzyme Activation/physiology
MH  - Exploratory Behavior/drug effects
MH  - Ganglia, Spinal/cytology/drug effects
MH  - Immunohistochemistry
MH  - Injections, Intradermal
MH  - Male
MH  - Motor Activity/drug effects
MH  - Nerve Tissue Proteins/biosynthesis
MH  - Neurons, Afferent/drug effects/enzymology
MH  - Nociceptors/drug effects
MH  - Pain/*metabolism/*psychology
MH  - Peripheral Nervous System/drug effects/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2006/11/07 09:00
MHDA- 2007/03/16 09:00
CRDT- 2006/11/07 09:00
PHST- 2006/06/16 00:00 [received]
PHST- 2006/08/24 00:00 [revised]
PHST- 2006/08/29 00:00 [accepted]
PHST- 2006/11/07 09:00 [pubmed]
PHST- 2007/03/16 09:00 [medline]
PHST- 2006/11/07 09:00 [entrez]
AID - S0306-4522(06)01170-5 [pii]
AID - 10.1016/j.neuroscience.2006.08.084 [doi]
PST - ppublish
SO  - Neuroscience. 2007 Jan 5;144(1):286-94. doi: 10.1016/j.neuroscience.2006.08.084. 
      Epub 2006 Nov 2.