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Abstract
The dorsal horn of the spinal cord is the location of the first synapse in pain pathways,
and as such, offers a very powerful target for regulation of nociceptive transmission
by both local segmental and supraspinal mechanisms. Descending control of spinal nociception
originates from many brain regions and plays a critical role in determining the experience
of both acute and chronic pain. The earlier concept of descending control as an "analgesia
system" is now being replaced with a more nuanced model in which pain input is prioritized
relative to other competing behavioral needs and homeostatic demands. Descending control
arises from a number of supraspinal sites, including the midline periaqueductal gray-rostral
ventromedial medulla (PAG-RVM) system, and the more lateral and caudal dorsal reticular
nucleus (DRt) and ventrolateral medulla (VLM). Inhibitory control from the PAG-RVM
system preferentially suppresses nociceptive inputs mediated by C-fibers, preserving
sensory-discriminative information conveyed by more rapidly conducting A-fibers. Analysis
of the circuitry within the RVM reveals that the neural basis for bidirectional control
from the midline system is two populations of neurons, ON-cells and OFF-cells, that
are differentially recruited by higher structures important in fear, illness and psychological
stress to enhance or inhibit pain. Dynamic shifts in the balance between pain inhibiting
and facilitating outflows from the brainstem play a role in setting the gain of nociceptive
processing as dictated by behavioral priorities, but are also likely to contribute
to pathological pain states.