Accessing the allodynia circuitry for persistent pain

Chronic pain affects about 30% of the population and significantly reduces quality of life because treatments are ineffective. Allodynia or touch-evoked pain is a particularly debilitating chronic pain symptom. A significant challenge to improving pain management is that the spinal neural circuitry that mediates allodynia is poorly understood. Recent efforts to characterise this circuitry have focused on traditional inflammatory and neuropathic pre-clinical pain models. However, these models do not emulate the chronicity of clinical pain. More recently developed hyperalgesic priming models mimic the transition from acute to chronic pain and are therefore more suited to study the allodynia circuitry relevant for persistent pain. Moreover, the allodynia circuitry in hyperalgesic priming models may actually be different because the underlying pathological plasticity is distinct from that identified in classical pre-clinical pain models.

I will determine whether Fos-EGFP transgenic mice can be used to gain morphological, electrophysiological and genetic ‘access’ to allodynia circuitry, in the clinically relevant persistent pain model of hyperalgesic priming.

This approach will generate pilot data for a larger grant application to characterise and facilitate future therapeutic targeting of allodynia circuitry.