The role of uninjured nerve in spinal nerve ligated rats points to an improved animal model of neuropathic pain.

L5 and L6 spinal nerve ligation (SNL) in rats leads to behavioral signs of neuropathic pain including mechanical allodynia. The purposes of this study were to investigate the role of the intact L4 spinal nerve in the development of mechanical allodynia following L5 and L6 SNL and, as a result, to develop a modified model of neuropathic pain. As a first set of experiments, in addition to tight ligation of the left L5 and L6 spinal nerves, the intact L4 spinal nerve was manipulated either (1) by gentle repeated stretching of the L4 spinal nerve immediately after L5 and L6 SNL or (2) by intermittent mechanical stimulation to the ipsilateral paw during the first week after SNL. Tactile sensitivity was measured by determining the foot withdrawal threshold before and after SNL. Mild irritation of L4 spinal nerve and application of mechanical stimuli to the ipsilateral paw significantly increased the development of mechanical allodynia after SNL. In a second set of experiments, SNL was produced by tightly ligating only the left L5 spinal nerve with or without a loop of 5-0 chromic gut placed loosely around the L4 spinal nerve. This additional L4 loop significantly increased long-lasting tactile sensitivity compared to L5 SNL alone. These results suggest that afferent activity of the intact L4 spinal nerve aids in the development of mechanical allodynia in the SNL model of neuropathic pain. The addition of a chromic gut loop around the intact L4 spinal nerve can augment the development of mechanical allodynia following SNL of L5. We propose this latter as a useful and practical animal model of neuropathic pain.