Concurrent Characterization of Local Spinal Cord Glucose Utilization and 3H-Phorbol 12, 13 Dibutylate Bindings in Inflammatory Pain State Induced by Paw Injection of Mustard Oil in Rats

The functional implication of complicated anatomical and neurochemical events of the spinal cord has been progressibly clarified. Although there are many evidences implicated as the primary sensory transmitter of acute pain in spinal cord, the reasons why the accelerates is not clear. We attempted to clarify the changes in local spinal cord glucose utilization (LSCGU), and protein kinase C (PKC) activation / translocation by MO (mustard oil) injection in relation to pain behaviour. Fourteen male Wistar rats were subjected to MO testing. The flinching of the injured paw was counted every 5min for the duration of 60min period. For the determination of LSCGU, 14C-2-deoxyglucose (14C-2DG) method was performed in the spinal cord at the same level as the 2nd and 5th cervical vertebrae for 60 min after MO injection. Simultaneously, using same frozen tissue, the binding sites of 3H-phorbol-dibutylate (PDBu) for PKC activity were determined by means of quantitative in vitro autoradiography. Following results were obtained : 1. The number of flinching after MO injection increased significantly in the MO group more than in the control group during 15min to 60min period. 2. 14C-2DG was increased significantly at laminae I-II and V-VI in the ipsilateral spinal cord at the same level as the 5th cervical vertebrae in the MO group than in the contralateral spinal cord in the MO group and bilateral spinal cord in the control group. 3. Bindings for 3H-PDBu at laminae I-II in the spinal cord were the densest, and binding at laminae I-II and V-VI in the ipsilateral spinal cord at the same level as the 5th cervical vertebrae in MO group than in the contralateral spinal cord in MO group and bilateral spinal cord in control group. The present study revealed the hyperalgesia in inflammatory pain by mustard Oil injection caused the spinal sensitization by the increase in LSCGU and the activation of PKC.