Translation Regulation in Central and Peripheral Pain Plasticity




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Pain under normal circumstances serves as a protective mechanism allowing recovery and survival. However, when pain becomes chronic, it no longer provides preservation but rather debilitation. Chronic pain is an important medical problem affecting greater than 33% of the population in America and current treatment options are only effective in a small percentage of the population and often accompanied with side effects. Determining the underlying molecular mechanisms of the maintenance and transition to chronic pain would lead us to developing new therapeutic treatments. Many studies suggest that translational control of gene expression is a key process for the regulation of plasticity in the nervous system. Multiple lines of evidence indicate that translation control plays a critical role in pathological pain plasticity, but precise gene targets have thus far not been elucidated. Brain-derived neurotrophic factor (BDNF) signaling through its cognate receptor, TrkB, is a well-known promoter of synaptic plasticity at nociceptive synapses in the dorsal horn of the spinal cord. However, the downstream effects contributing to the maintenance of a chronic pain state remain elusive. The goal of our research is to further understand the biochemical mechanisms driving chronic pain using pharmacological techniques and transgenic mice. Our work provides novel insight into mechanisms driving pain chronification and defines MNK regulation of eIF4E phosphorylation as a key target for pain therapeutics.



Neuroplasticity, Chronic pain, Pain—Treatment, Gene expression, Eukaryotic cells, Phosphorylation


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