[Abstract Title]. - Society for Neuroscience

Title: Changes in TRPV1 function in A-fiber neurons after nerve injury
Authors: *D. VILCEANU, C. L. STUCKY;
Dept Cell Biol, Neurobiol & An, Med. Col. Wisconsin, Milwaukee, WI
Abstract: Clinical manifestations of peripheral nerve injury include hypersensitivity to heat and
mechanical stimuli, but the underlying molecular mechanisms are not yet clear. The TRPV1
channel is an important player that contributes to both heat hypersensitivity and pain sensation as
it is activated by noxious heat ( >42°C) and by many endogenous inflammatory chemicals
including protons. TRPV1 is normally expressed mainly in small-diameter ( 26 um) which likely have A fiber
axons. We assessed heat responsiveness by applying a fast ramp of heated buffer (24 to 50°C in
3 sec). The criterion for a heat response was a rapid inward current > 100 pA that exhibited a
clear heat threshold.
Among medium-large neurons from naive controls, only 9% (4/45) of L3/L4 DRG neurons
responded to heat, whereas in sham-operated mice, 15.4% (8/52) neurons responded to heat.
After SNL injury, the percentage of heat responsive neurons from the injured L4 ganglia
decreased to just 2% (1/48, p = 0.03 compared with sham neurons). Surprisingly however, the
percentage of heat-responsive neurons from the adjacent L3 DRG was only 6% (3/49) and not
increased compared to either the naive or sham controls. All heat-evoked responses appeared to
be entirely due to TRPV1 activation because they had an average heat threshold of 44±0.2°C.
These data indicate that spinal nerve ligation in mice does not alter TRPV1 function in A-fiber
type neurons adjacent to the injury and thus, TRPV1 does not likely contribute to nerve injuryinduced
evoked heat hyperalgesia.
Disclosures: D. Vilceanu, None; C.L. Stucky, None.
Poster
268. Neuropathic Pain Mechanisms: Ion Channels
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 268.6/GG3