Pain Makes CaMKII Go Up And Down

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Pain Makes CaMKII Go Up And Down

http://www.medicalnewstoday.com/medicalnews.php?newsid=41893

Aparticularly intense painful stimulus enhances the sensation evoked

by subsequent noxious stimuli. This hyperalgesia may result from

facilitation of sensory neurotransmission in the spinal cord, perhaps

by mechanisms similar to synaptic plasticity in other pathways. In

this week's Journal, Larsson and Broman used immunolabeling of

calcium/calmodulin-dependent kinase II (CaMKII) to track the

associated modulation of spinal cord pathways. The translocation of

autophosphorylated CaMKII to the postsynaptic density makes it one

marker of synaptic plasticity. The authors injected rat hindpaws with

capsaicin to induce hyperalgesia. Transganglionic tracing of the

capsaicin injection site marked the nonpeptidergic class of

nociceptors, but not peptidergic nociceptive neurons that express

substance P and calcitonin generelated peptide. Phosphorylated CaMKII

more than doubled in dorsal horn synapses formed by peptidergic

neurons and fell by about one-half in synapses formed by labeled,

nonpeptidergic neurons. In low-threshold mechanoreceptor neurons,

CaMKII expression did not change with capsaicin treatment.

The Journal of Neuroscience April 2006

Max Larsson and Jonas Broman