Brain research
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Peripheral tissue injury results in a change in the excitability of spinal dorsal horn neurons, central sensitization, and the behavioral correlate, hyperalgesia. It is proposed here that a dynamic balance exists between excitatory and inhibitory synaptic input to the spinal dorsal horn that functions to prevent central sensitization following brief, mild, noxious stimulation. Following more severe stimulation and injury, there is a loss of these inhibitory mechanisms that allow central sensitization to proceed. ⋯ It is suggested that this attenuation, whether or not expressed, prevents a significant portion of deep dorsal horn neurons from becoming sensitized to C-fiber input. This functions to prevent central sensitization when the noxious stimulus does not produce inflammation and it is not beneficial to the animal to become hyperalgesic (i.e., to alter its behavior in order to protect an injured limb and reduce painful sensations). Following injury-producing tissue damage and inflammation the mechanisms that produce the attenuation are reduced, with a concomitant increase in excitation to electrical and natural stimuli, suggesting that the attenuation is inhibitory modulation of nociceptive input and injury results in a disinhibition producing an increase in excitability and central sensitization.