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Evidence suggests that there are both nociceptive and neuropathic components of cancer-induced pain (CIP). We have observed that changes in intrinsic membrane properties and excitability of normally non-nociceptive Aβ sensory neurons are consistent in rat models of peripheral neuropathic pain (NEP) and CIP. This has prompted a comparative investigation of the intracellular electrophysiological characteristics of sensory neurons and of the ultrastructural morphology of the dorsal horn in rat models of NEP and CIP. NEP model rats were induced with a polyethylene cuff implanted around a sciatic nerve. CIP model rats were induced with MRMT-1 rat breast cancer or MATLyLu rat prostate cancer cells implanted into the distal epiphysis of a femur. Behavioural evidence of nociception was detected using von Frey tactile assessment. Aβ-fibre low threshold mechanoreceptor (LTM) neurons in both CIP and NEP models exhibited slower dynamics of action potential (AP) genesis, including a wider AP duration and lower AP amplitude compared to those in control animals. Enhanced excitability of Aβ-fibre LTM neurons was also observed in CIP and NEP models. Furthermore, both CIP and NEP models showed abundant abnormal axonal sprouting in bundles of myelinated axons in the ipsilateral spinal laminae IV and V. The patterns of changes in Aβ DRG neurons show consistency between rat models of CIP and NEP. In addition, sprouting in the lumbar spinal cord was observed in samples from both models. These findings add to the body of evidence that animal models of CIP and NEP share features that may contribute to the peripheral and central sensitization and tactile hypersensitivity in both pain states.

molecular pain

Cancer pain and neuropathic pain are associated with A<b><i>β</i></b> sensory neuronal plasticity in dorsal root ganglia and abnormal sprouting in lumbar spinal cord

Cancer pain and neuropathic pain are associated with Aβ sensory neuronal plasticity in dorsal root ganglia and abnormal sprouting in lumbar spinal cord