The synaptic connectivity that underlies the noxious transmission and modulation within the superficial dorsal horn of the spinal cord.
Noxious stimuli can usually cause the aversive sensations, pain and itch. The initial integration of such noxious information occurs in the superficial dorsal horn of the spinal cord (SDH), which is very important for understanding pain sensation and developing effective analgesic strategies. The circuits formed by pools of neurons and terminals within SDH are accepted as the platform for such complicated integrations and are highly plastic under conditions of inflammatory or neuropathic pain. Recent literature offers a complicated, yet versatile view of SDH intrinsic circuits with both inhibitory and excitatory components. However, our knowledge about the adaptative regulation of SDH local circuits is still far from sufficient due to the incomplete understanding of their organization as they are intermingled with primary afferent fibers (PAFs), poorly understood or identified SDH neurons, somehow contradictory data for descending control systems. A more positive view emphasizes abundant modern data on SDH neuron morphology and physiology riding on the back of significant technological advancements used in neuroscience. Reviewing the current literature on this topic thus produced an integrated understanding of SDH neurons and the SDH local circuits involved in noxious transmission and modulation.
Wu
Sheng-Xi
SX
Department of Anatomy, Histology and Embryology and K. K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an 710032, PR China.
Wang
Wen
W
Li
Hui
H
Wang
Ya-Yun
YY
Feng
Yu-Peng
YP
Li
Yun-Qing
YQ
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D009475:Neurons, Afferent / Q000166:cytology / Q000502:physiology; D009476:Neurons, Efferent / Q000166:cytology / Q000502:physiology; D013116:Spinal Cord / Q000033:anatomy & histology / Q000502:physiology; D013569:Synapses / Q000378:metabolism / Q000648:ultrastructure; D009435:Synaptic Transmission / Q000502:physiology*