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Calcium/calmodulin-dependent protein kinase II (CaMK II) is found throughout the CNS. It regulates calcium signaling in synaptic transmission by phosphorylating various proteins, including neuronal membrane receptors and intracellular transcription factors. Inflammation or injuries to peripheral tissues cause long-lasting increases in the responses of central nociceptive neurons to innocuous and noxious stimuli. This change can occur independently of alterations in the responsiveness of primary afferent neurons and has been termed central sensitization. Central sensitization is a form of activity-dependent plasticity and results from interactions in a set of intracellular signaling pathways, which modulate nociceptive transmission. Here we demonstrate an increased expression and phosphorylation of CaMK II in rat spinal dorsal horn neurons after noxious stimulation by intradermal injection of capsaicin. Local administration of a CaMK II inhibitor in the spinal cord significantly inhibits the enhancement of responses of spinal nociceptive neurons and changes in exploratory behavior evoked by capsaicin injection. In addition, spinal CaMK II activity enhances phosphorylation of AMPA receptor GluR1 subunits during central sensitization produced by capsaicin injection. This study reveals that CaMK II contributes to central sensitization in a manner similar to its role in the processes underlying long-term potentiation.
Fang et al. (Wed,) studied this question.