The liberation of fractalkine in the dorsal horn requires microglial cathepsin S.

ABSTRACT: Understanding of the sequence and nature of the events that govern neuron-microglia communication is critical for the discovery of new mechanisms and targets for chronic pain treatment. The neuronal chemokine fractalkine (FKN) and its microglial receptor CX3CR1 may mediate such a function in the dorsal horn of the spinal cord after cleavage of the extracellular domain of this transmembrane chemokine by a protease. Here we report that in neuropathic rat dorsal horn, with dorsal root-attached preparations, soluble FKN (sFKN) contents are increased in the superfusates collected after noxious-like electrical stimulation of ipsilateral primary afferent fibers. The increase of sFKN is prevented by morpholinurea-leucine-homophenylalanine-vinyl sulfone-phenyl (LHVS), an irreversible inhibitor of c

SUBMITTER: Clark AK 

PROVIDER: S-EPMC2698289 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature