The Journal of Neuroscience, February 8, 2006, ():
Disinhibition Opens the Gate to Pathological Pain Signaling in Superficial Neurokinin 1 Receptor-Expressing Neurons in Rat Spinal Cord
J. Neurosci. Torsney and MacDermott
26: 1833
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplemental Figure 1. Schematic summarizing an hypothesis for the underlying dorsal horn circuitry mediating afferent input onto lamina I NK1R+ neurons. Lamina I NK1R+ neurons receive direct monosynaptic input from Aδ and C fibers and polysynaptic input from Aβ fibers. Inhibitory interneurons act directly on some or all excitatory interneurons in the polysynaptic pathway that express the NMDA receptor. Inhibitory interneurons hyperpolarize the excitatory interneurons and maintain the Mg2+ block and prevent current flow through the NMDA receptor rendering the synapses less effective. This prevents activation of the NK1R+ neuron by the polysynaptic input. Inhibition may be tonically active or, as illustrated, driven by primary afferent Aβ fibers. Disinhibition unmasks the NMDA receptor dependent polysynaptic pathway and reveals substantial polysynaptic Aβ fiber input to lamina I NK1R+ neurons.
