[Abstract Title]. - Society for Neuroscience

1 Orthopaedic surgery, Kyushu Univ., Fukuoka, Japan; 2 Dept. of Integrative Physiol., Grad. Sch.
of Med. Sciences, Kyushu Univ., Fukuoka, Japan; 3 Dept. of Anesthesiol., Sapporo Med.
University, Sch. of Med., Sapporo, Japan
Abstract: Cancer-induced bone pain is a major clinical problem for which current treatments
lack satisfactory efficiency. We investigated pain behavioral changes and plasticity of neural
excitatory synaptic input to the superficial dorsal horn in a murine model of cancer-induced bone
pain.
A mouse model of bone cancer pain was produced by the implantation of osteosarcoma cells
(NCTC2472, 10×10 5 in 20κL of medium) into the mouse femur. The first of all, bone histology
and pain-related behaviors were assessed on day 7 and 14 after sarcoma injection. Another
behavioral changes were tested by assessing the development of mechanical allodynia and
thermal allodynia at hind paw only in the model mice that had apparent pain-related behaviors.
Plantar mechanical and thermal allodynia was assessed by von Frey test and plantar test. When
there were significant behavioral alterations in the model mice, compared to naïve,
electrophysiological experiments were carried out on day 15-21 after surgery. Voltage patchclamp
recordings from superficial dorsal horn neurons of the slices at lumbar spinal cord level
(L3-5) were performed.
The behavioral studies showed that mechanical, but not thermal, pain threshold of hind paw,
over the lesion level, was significantly increased with hind paw lifting and flinching which were
typical behavioral signs of spontaneous pain. Electrophysiological recordings demonstrated
significant increase of both frequency and amplitude of spontaneous excitatory postsynaptic
current (sEPSC), respectively, by 157% and 118%.
These results suggest that central sensitization was occurred due to the increased excitatory
synaptic input by cancer-related spontaneous pain stimulation, result in allodynia and
hypersensitivility. The threshold and amplitude of root-evoked EPSCs should be tested for the
next step.
Disclosures: Y. Yanagisawa , None; H. Furue, None; T. Kawamata, None; D. Uta, None; A.
Namiki, None; Y. Iwamoto, None; M. Yoshimura, None.
Poster
268. Neuropathic Pain Mechanisms: Ion Channels
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 268.4/GG1
Topic: D.08.l. Neuropathic pain: Mechanisms
Title: Anti-allodynic effect of the HCN antagonist, ZD7288, after nerve injury in HCN1-null
mice