Topic: spinal dorsal horn

Neuropathic pain is evoked by an injury to the somatosensory system at the peripheral or central nervous system level leading to direct changes in neuronal activity. Moreover, there is a large body of evidence that changes occurring in primary peripheral sensory neurons also alter secondary central circuits thus causing hyperalgesia and allodynia. The latter are hallmarks of neuropathic pain and recent work suggests that both of those sensory abnormalities depend on alterations in spinal dorsal horn circuits likely caused by a loss of local inhibition. However, the molecular mechanisms that le

Pain expectation is known to influence pain perception, but the underlying neuronal mechanisms remain unclear. While the motor role of the corticospinal tract is well characterized, only recently was it established that the corticospinal neurons originating from the primary somatosensory cortex (S1-CSNs) specifically contact the sensory region of the spinal cord, providing top-down regulation of sensations including pain. S1-CSNs neurons are therefore ideally positioned to modulate spinal nociception based on sensory representations and expectations. To test whether S1-CSNs activity is modulat

Dynamic reorganization of neuronal circuits in the spinal dorsal horn is assumed to cause sensitization in the neuropathic pain. In our previous study, brain-enriched guanylate kinase associated-protein (BEGAIN) was identified as an increased protein in the spinal dorsal horn in the neuropathic pain and the mechanical allodynia was attenuated in the BEGAIN-knockout mice. BEAGIN-expressing neurons have not yet been identified because BEGAIN protein is detected in highly localized dendritic regions, not in the cell body. To identify BEGAIN-expressing neurons, double in situ hybridization with RN