Despite intensive effort and resulting gains in understanding the mechanisms underlying neuropathic pain, limited success in therapeutic approaches have been attained.
Authors in the journal PNAS define the causative role of endoplasmic reticulum (ER) stress on selective modulation of pain signaling.
High levels of ER stress and neuropathic pain in diabetic animals are reduced using ER stress blockers.
In healthy animals, turning on the ER stress signal transduction cascade generates an immediate but lasting and site restricted painful phenotype, which is reversible by ER stress blockers.
This previously unnoticed mechanism explains the broad lack of efficacy of available analgesics and should ignite the discovery of a new generation of therapeutics that do not directly quell ion channel or neurotransmitter activity.
http://www.pnas.org/
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