In pain transmission, the 'gate control theory' by Melzack and Wall proposes that activation of Aβ fibers inhibits pain. What is the synaptic mechanism in the dorsal horn?
- A Aβ fiber activation excites inhibitory interneurons (substantia gelatinosa, lamina II) that presynaptically inhibit C-fiber and Aδ-fiber terminals, reducing nociceptive transmission to projection neurons ✓
- B Aβ fibers directly hyperpolarize C-fiber cell bodies in the dorsal root ganglion via gap junctions
- C Aβ fibers activate descending serotonergic fibers from raphe nuclei that postsynaptically inhibit wide-dynamic-range neurons
- D Aβ fibers release substance P that competes with nociceptor substance P at NK1 receptors
Explanation
Gate control theory proposes a 'gate' in the dorsal horn (substantia gelatinosa, lamina II). Large-diameter myelinated Aβ mechanoreceptor fibers and small-diameter C/Aδ nociceptors both project to wide-dynamic-range (WDR) projection neurons (lamina V) and to inhibitory interneurons in lamina II. Aβ fiber activity excites these inhibitory interneurons (using enkephalins/GABA), which presynaptically inhibit nociceptive C/Aδ terminals — closing the gate. C-fiber activity inhibits these same interneurons — opening the gate. This explains why rubbing a hurt area provides relief and is the basis for TENS therapy.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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