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Nociceptor sensitization is a process triggered by proinflammatory factors that result in a significant increase in neuronal excitability by affecting both the threshold and frequency of action potential firing. The increased sensory neu- ron activity is due to a metabolic change produced by the activation of intracellular signaling cascades that usually alter the expression and functionality of molecular sensors present in the neuronal surface, i.e. ion channels and metabotropic receptors. Cumulative evidence is showing that inflammatory sensitization of nociceptors is significantly contributed by an enhanced expression of ion channels that directly influence neuronal excitability. Furthermore, recent data indicates that mobilization and regulated exocytosis of a ready-to-go vesicular population of channels as a pivotal event underlying acute inflammatory sensitization of sensory neurons; whereas an increment in transcription and/or translation and traffick- ing is involved in chronic neuronal sensitization. Therefore, identification of the molecular components involved in chan- nel trafficking and exocytosis in the inflamed terminal may provide new strategies for attenuating nociceptor sensitization and their consequences, namely hyperalgesia and allodynia.

Contribution of Ion Channel Trafficking to Nociceptor Sensitization