Polysomal profiling of spinal cells after peripheral nerve injury

Neuropathic pain is evoked by an injury to the somatosensory system at the peripheral or central nervous system level leading to direct changes in neuronal activity. Moreover, there is a large body of evidence that changes occurring in primary peripheral sensory neurons also alter secondary central circuits thus causing hyperalgesia and allodynia. The latter are hallmarks of neuropathic pain and recent work suggests that both of those sensory abnormalities depend on alterations in spinal dorsal horn circuits likely caused by a loss of local inhibition. However, the molecular mechanisms that lead to these circuit changes are still poorly understood thus hampering the identification of new promising druggable targets. To redress this, we characterized gene expression changes occurring in different neuronal and non-neuronal spinal cell populations after peripheral nerve injury (PNI) employing the highly sensitive Translating Ribosome Affinity Purification (TRAP) method. Through Differential Gene Expression Analysis, we identified gene expression changes at different time points post nerve injury that alter the proteome of the analyzed spinal cell types. Collectively, these data show the specificity and complexity of the response to PNI and provide novel insights into transcriptional as well as translational changes associated with neuropathic pain. The affected genes are potential candidate targets for the treatment of the chronic pain.