Our objective is to understand how axonal transport and local protein synthesis contribute to hyperexcitability exhibited by damaged neurons leading to neuropathic pain states.

Spinal muscular atrophy (SMA) is an autosomal disease caused by deletion or mutation(s) of thesurvival motor neuron 1 (SMN1) gene. A highly homologous gene, SMN2, is present in all patients but yields low levels of the full-length SMN protein.

The objective of this study is to determine how the capacity for localized protein synthesis in axons is altered by injury.