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Environmental influences found to have role for development and function of the pain system

by electrophysiologically recording reflex responses to electrical stimulation of the afferent nerve fibers that had innervated the injured tissue. Spinal preparations obtained from rats with an injured paw showed greatly enhanced neuronal responses compared with those obtained from control rats.

Laird also has described how the intracellular signaling pathways and molecular mechanisms known to be critical for classical learning and retention of memories in the hippocampus seem to be involved in spinal "memories" of painful injury.

The scientists have shown in both rats and mice that extracellular signaling-related kinases are activated in the spinal cord by painful stimuli with a time course that matches the maintenance of hypersensitivity. The activated kinases translocate to the neuronal nuclei, thereby enabling an influence on gene expression. Blockers of this activation dose-dependently reduce the hypersensitivity observed in behavioral tests in mice.

The results also provide a key to understand the more general problem of how the body constitution is represented in the CNS. It is envisioned that knowledge about the cellular mechanisms underlying the storage of painful events will allow artificial down regulation of pain sensitivity and thereby open up for the development of new therapeutic methods to relieve chronic pain.


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Contact: Dawn McCoy
dawn@sfn.org
202-462-6688
Society for Neuroscience
10-Nov-2003


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