Melzack and Wall proposed the gate-control theory in 1965. According to this theory, a neural mechanism in the dorsal horn of the spinal cord acts as a gate; this gate increases or decreases the flow of nerve impulses from the peripheral fibers to the centra nervous system (CNS). The extent to which the gate enhances or reduces sensory transmission is determined by the relative activity of the large diameter (A-beta) and small diameter (A-delta and C) fibers. When the amount of information passing through the gate exceeds a critical level, it activates the neural areas responsible for pain sensation. The most likely site where spinal gating occurs is the substantia gelatinosa. The cells in lamina V of the spinal cord may act as transmission cells in the mechanism of pain sensation.
This model of Melzack and Wall was criticized because it emphasized presynaptic control and failed to predict the complex pattern of facilitation and inhibition observed in dorsal horn cells. In the revised model of Melzack and Wall, substantia gelatinosa contains both excitatory and inhibitory cells which project to he transmission cells. Central control mechanisms in the brain also modulate pain via corticifugal fibers that carry signals from the brain to the gate in the spinal cord so that nociception is inhibited.
Modulation by Descending Pathways
It has been shown that electrical stimulation of the periaqueductal gray matter of the rat brain and human brain results in profound analgesia. Nucleus raphae magnus, which is located in the pons and rostral medulla, receives projections from the periaqueductal gray. High density of projections from the nucleus raphae magnus to the substantia gelatinosa has been observed. These projections descend through the dorsolateral funiculus of the spinal cord. The analgesia evoked by the stimulation of periaqueductal gray is dependent on this raphae-spinal pathway.
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