The superficial dorsal horn, particularly substantia gelatinosa (SG) in the spinal cord, receives inputs from small-diameter primary afferents that predominantly convey noxious sensation. This sensory information via the high-threshold Aδ and C afferents is modified and integrated in SG, and consequently regulates the outputs of projection neurons located in lamina I and laminae IV-V. Recent studies using slice and in vivo patch-clamp recordings indicate that the sensory inputs to SG are functionally reorganized during post-natal development. Even in the mature state, the synaptic connectivity and receptor expression in SG can be altered easily following peripheral tissue damage. In addition, the descending pain inhibitory system to SG is also modified under certain pathological conditions. Considering that the pain system is phylogenetically primitive, it is, therefore, not surprising that the system easily exhibits a plastic change in response to inflammation or nerve damage. Because such plastic changes in the neuronal circuit or receptor expression in SG are now generally accepted to be one of the explanations for the induction of pathological pain, SG is thought to be a primary therapeutic target for chronic pain. We review here recent results demonstrating plastic changes in SG under pathological conditions.
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