Reduction in inhibitory control is sufficient to generate hyperalgesia in a spiking model of nociceptive integration in the superficial dorsal horn
© Sousa et al; licensee BioMed Central Ltd. 2013
Published: 8 July 2013
The spinal cord's dorsal horn is a major termination site for primary afferents carrying sensory information from the periphery. The superficial dorsal horn (SDH, laminae I and II), in particular, receives inputs from nociceptive C and Aδ fibers, and have an important role in relaying and processing nociceptive information. This work focuses on the pain condition named hyperalgesia, characterized by an increased response to a stimulus that is normally painful. Much is still unknown regarding the central mechanisms giving rise to this condition.
This model shows that mechanisms interfering with the balance between excitation/inhibition and reducing, temporarily or chronically, the feed-forward inhibitory control in the SDH have the potential to give rise to hyperalgesia. Understanding how this pain condition occurs provides important information on how to reverse pathological situations. This work was supported by grant SFRH/BD/60690/2009 from FCT.
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