PMID- 19524560
OWN - NLM
STAT- MEDLINE
DCOM- 20091009
LR  - 20171116
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1284
DP  - 2009 Aug 11
TI  - Acute and chronic effects of neurotrophic factors BDNF and GDNF on responses 
      mediated by thermo-sensitive TRP channels in cultured rat dorsal root ganglion 
      neurons.
PG  - 54-67
LID - 10.1016/j.brainres.2009.06.014 [doi]
AB  - Neurotrophic factors (NTFs), beside regulating neuronal survival in the central 
      and peripheral nervous system, are also involved in the modulation of neuronal 
      function in the adult animal. Both brain-derived neurotrophic factor (BDNF) and 
      glial cell-derived neurotrophic factor (GDNF) levels are altered in pathological 
      pain states, and exogenous BDNF and GDNF have multiple effects on pain behavior, 
      depending on the animal model (i.e. inflammatory vs. neuropathic). Thermally 
      gated TRP channels TRPM8, TRPA1 and TRPV1 play a significant role in pain 
      signaling and their pattern and level of expression as well as their biophysical 
      properties are altered in chronic pain states. Our aim was to investigate the 
      effect of long-term and acute exposure to BDNF and GDNF on the functional 
      expression of these thermoTRP channels in cultured rat dorsal root ganglion (DRG) 
      neurons. We found that while BDNF treatment primarily increased the fraction of 
      capsaicin-sensitive (TRPV1-expressing) neurons, GDNF exposure led to an increase 
      in the allyl isothiocyanate (AITC)-responding (TRPA1-expressing) population. 
      Moreover, BDNF treatment increased the amplitude of the response to both AITC and 
      capsaicin. Acute treatment with both NTFs leads to a reduction in the magnitude 
      of tachyphylaxis to noxious stimuli (heat and AITC). Overall, our data provides 
      evidence for a role of BDNF and GDNF in regulating the pattern of expression and 
      level of activity of the transducer channels TRPA1 and TRPV1, leading to enhanced 
      neuronal sensitivity to painful stimuli and increased co-expression of thermoTRP 
      channels.
FAU - Ciobanu, Cristian
AU  - Ciobanu C
AD  - Department of Animal Physiology and Biophysics, Faculty of Biology, University of 
      Bucharest, Splaiul Independentei 91-95, 050095 Bucharest, Romania.
FAU - Reid, Gordon
AU  - Reid G
FAU - Babes, Alexandru
AU  - Babes A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090612
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Allyl Compounds)
RN  - 0 (Ankyrins)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calcium Channels)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (Isocyanates)
RN  - 0 (Sensory System Agents)
RN  - 0 (TRPA1 Cation Channel)
RN  - 0 (TRPC Cation Channels)
RN  - 0 (TRPM Cation Channels)
RN  - 0 (TRPV Cation Channels)
RN  - 0 (Trpa1 protein, rat)
RN  - 0 (Trpm8 protein, rat)
RN  - 0 (Trpv1 protein, rat)
RN  - 0 (allyl isocyanate)
RN  - S07O44R1ZM (Capsaicin)
SB  - IM
MH  - Allyl Compounds/pharmacology
MH  - Animals
MH  - Ankyrins
MH  - Brain-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Calcium Channels/drug effects/metabolism
MH  - Capsaicin/pharmacology
MH  - Cells, Cultured
MH  - Cold Temperature
MH  - Ganglia, Spinal/drug effects/*metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Glial Cell Line-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Hot Temperature
MH  - Humans
MH  - Isocyanates/pharmacology
MH  - Pain/chemically induced/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Sensory System Agents/pharmacology
MH  - TRPA1 Cation Channel
MH  - TRPC Cation Channels/drug effects/*metabolism
MH  - TRPM Cation Channels/drug effects/metabolism
MH  - TRPV Cation Channels/drug effects/metabolism
EDAT- 2009/06/16 09:00
MHDA- 2009/10/10 06:00
CRDT- 2009/06/16 09:00
PHST- 2009/03/18 00:00 [received]
PHST- 2009/06/05 00:00 [revised]
PHST- 2009/06/06 00:00 [accepted]
PHST- 2009/06/16 09:00 [entrez]
PHST- 2009/06/16 09:00 [pubmed]
PHST- 2009/10/10 06:00 [medline]
AID - S0006-8993(09)01186-X [pii]
AID - 10.1016/j.brainres.2009.06.014 [doi]
PST - ppublish
SO  - Brain Res. 2009 Aug 11;1284:54-67. doi: 10.1016/j.brainres.2009.06.014. Epub 2009 
      Jun 12.