EFFECTS OF INJURY DISCHARGE ON THE PERSISTENT EXPRESSION OF SPINAL-CORD FOS-LIKE IMMUNOREACTIVITY PRODUCED BY SCIATIC-NERVE TRANSECTION IN THE RAT

We recently reported that peripheral nerve injury produced by sciatic nerve transection induces a persistent increase in the expression of t he immunoreactive Fos protein product of the c-fos proto-oncogene, an indicator of neuronal activity, in the lumbar spinal cord of the rat a nd that local anesthetic blockade of the peripheral neuroma attenuates this long-term expression of Fos6,7. In addition to the sustained act ivity of the injured afferents, the nerve transection itself results, acutely, in a massive injury-induced neural discharge. In this study w e evaluated the effect of blocking this massive injury discharge on th e persistence of Fos expression. Just prior to nerve transection we ap plied the short-acting local anesthetic, lidocaine, to the sciatic ner ve. Control injections were made subcutaneously on the dorsum of the n eck. We report that injection of the local anesthetic, by either route , significantly reduced the number of fos-like immunoreactive neurons at 2 days after nerve transection. The effect was only observed on neu rons in the superficial dorsal horn. These results indicate that along with sustained activity of injured afferents and of reorganization of central circuits after injury, the initial brief discharge at the tim e of nerve injury contributes to a prolonged increase in the activity of spinal cord neurons.