PMID- 24099268
OWN - NLM
STAT- MEDLINE
DCOM- 20140717
LR  - 20211203
IS  - 1744-8069 (Electronic)
IS  - 1744-8069 (Linking)
VI  - 9
DP  - 2013 Oct 8
TI  - Activation of mammalian target of rapamycin mediates rat pain-related responses 
      induced by BmK I, a sodium channel-specific modulator.
PG  - 50
LID - 10.1186/1744-8069-9-50 [doi]
AB  - The mammalian target of rapamycin (mTOR) is known to regulate cell proliferation 
      and growth by controlling protein translation. Recently, it has been shown that 
      mTOR signaling pathway is involved in long-term synaptic plasticity. However, the 
      role of mTOR under different pain conditions is less clear. In this study, the 
      spatiotemporal activation of mTOR that contributes to pain-related behaviors was 
      investigated using a novel animal inflammatory pain model induced by BmK I, a 
      sodium channel-specific modulator purified from scorpion venom. In this study, 
      intraplantar injections of BmK I were found to induce the activation of mTOR, p70 
      ribosomal S6 protein kinase (p70 S6K) and eukaryotic initiation factor 4E-binding 
      protein 1 (4E-BP1) in rat L5-L6 spinal neurons. In the spinal cord, mTOR, p70 S6K 
      and 4E-BP1 were observed to be activated in the ipsilateral and contralateral 
      regions, peaking at 1-2 h and recovery at 24 h post-intraplantar (i.pl.) BmK I 
      administration. In addition, intrathecal (i.t.) injection of rapamycin - a 
      specific inhibitor of mTOR - was observed to result in the reduction of 
      spontaneous pain responses and the attenuation of unilateral thermal and 
      bilateral mechanical hypersensitivity elicited by BmK I. Thus, these results 
      indicate that the mTOR signaling pathway is mobilized in the induction and 
      maintenance of pain-activated hypersensitivity.
FAU - Jiang, Feng
AU  - Jiang F
AD  - Lab of Neuropharmacology & Neurotoxicology, Shanghai University, 200444 Shanghai, 
      P,R, China. yhji@staff.shu.edu.cn.
FAU - Pang, Xue-Yan
AU  - Pang XY
FAU - Niu, Qing-Shan
AU  - Niu QS
FAU - Hua, Li-Ming
AU  - Hua LM
FAU - Cheng, Ming
AU  - Cheng M
FAU - Ji, Yong-Hua
AU  - Ji YH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131008
PL  - United States
TA  - Mol Pain
JT  - Molecular pain
JID - 101242662
RN  - 0 (Scorpion Venoms)
RN  - 0 (Sodium Channel Blockers)
RN  - 0 (Sodium Channels)
RN  - 0 (makatoxin I)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Male
MH  - Pain/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Scorpion Venoms/*pharmacology
MH  - Signal Transduction/drug effects
MH  - Sodium Channel Blockers/pharmacology
MH  - Sodium Channels/*drug effects
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC3842742
EDAT- 2013/10/09 06:00
MHDA- 2014/07/18 06:00
PMCR- 2013/10/08
CRDT- 2013/10/09 06:00
PHST- 2012/10/11 00:00 [received]
PHST- 2013/09/24 00:00 [accepted]
PHST- 2013/10/09 06:00 [entrez]
PHST- 2013/10/09 06:00 [pubmed]
PHST- 2014/07/18 06:00 [medline]
PHST- 2013/10/08 00:00 [pmc-release]
AID - 1744-8069-9-50 [pii]
AID - 10.1186/1744-8069-9-50 [doi]
PST - epublish
SO  - Mol Pain. 2013 Oct 8;9:50. doi: 10.1186/1744-8069-9-50.