Endogenous galanin is required for the full expression of central sensitization following peripheral nerve injury.

The neuropeptide galanin is known to be involved in nociceptive sensory processing in the spinal cord. We have attempted to better characterise the function of endogenous galanin in nociceptive signalling by examining a mouse strain carrying a loss of function mutation in the galanin gene (gal-/-). Galanin expression is significantly up-regulated following damage to a peripheral nerve. To address what effect this up-regulation has on spinal cord excitability we have examined wild type (gal+/+) and gal-/- mice 3 days after complete transection of the sciatic nerve using an electrophysiological paradigm, the flexor withdrawal reflex. We demonstrate that the up-regulation of galanin has no direct effect on basal spinal excitability after nerve injury. However, galanin is shown to be a crucial neuromodulator involved in the development of the central sensitization as both windup and the facilitation of spinal reflexes following conditioning stimulation are significantly impaired in gal-/- mice following peripheral nerve injury.