Basic neurochemistry of central sensitization

Abstract

Peripheral inflammation or injury can often result in enhanced transmission of sensory input through the spinal cord dorsal horn, this is termed central sensitization. This phenomenon, which results in pain responses from uninjured tissue, is a major clinical problem. Pharmacologic treatments must address neurochemical events in the spinal cord that contribute to central sensitization and resultant pain. This study reviews injury-induced glutamate receptor activation, changes in Ca²⁺ flux, and induction of calcium-dependent second messenger cascades occurring within central nociceptive afferent terminals and spinal nociceptive neurons in an attempt to explain and predict some of the relevant clinical pharmacology.