Gate control theory

When one experiences a negative sensation, such as pain from a bump or an itch from a bug bite, a common reaction is an attempt to eliminate the feeling by rubbing the painful bump or scratching the itchy bite. Gate control theory asserts that activation of nerves that do not transmit pain signals, called nonnociceptive fibers, can interfere with signals from pain fibers, thereby inhibiting pain. It is proposed that both small-diameter (pain-transmitting) and large-diameter (touch-, pressure-, and vibration- transmitting) afferent nerve fibers carry information from the site of the injury to two destinations in the dorsal horn: 1. Transmission Cells that carry the pain signal up to the brain, and 2. Inhibitory Interneurons that impede transmission cell activity. Activation of transmission cells occurs from both excitatory small-diameter and excitatory large-diameter fibers. However, activation of the inhibitory interneurons varies: large-diameter fibers excite the interneuron, which ultimately reduces transmission cell firing, whereas small-diameter fibers inhibit the inhibitory interneuron which lessens the inhibitory input to the transmission cell. Therefore, less pain is felt (via reduced transmission cell activity) when more activity in large-diameter fibers (touch-, pressure-, and vibration- transmitting) occurs relative to the activity in small-diameter (pain-transmitting) fibers. The peripheral nervous system has centers at which pain stimuli can be regulated. Some areas in the dorsal horn of the spinal cord that are involved in receiving pain stimuli from Aδ and C fibers, called laminae, also receive input from Aβ fibers. An inhibitory connection may exist with Aβ and C fibers, which may form a synapse on the same projection neuron. The same neurons may also form synapses with an inhibitory interneuron that also synapses on the projection neuron, reducing the chance that the latter will fire and transmit pain stimuli to the brain (image on the right). The inhibitory interneuron fires spontaneously. The C fiber's synapse would inhibit the inhibitory interneuron, indirectly increasing the projection neuron's chance of firing. The Aβ fiber, on the other hand, forms an excitatory connection with the inhibitory interneuron, thus decreasing the projection neuron's chance of firing (like the C fiber, the Aβ fiber also has an excitatory connection on the projection neuron itself). Thus, depending on the relative rates of firing of C and Aβ fibers, the firing of the nonnociceptive fiber may inhibit the firing of the projection neuron and the transmission of pain stimuli. == History and legacy ==

and Patrick Wall introduced their "gate control" theory of pain in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the spinal cord: transmission cells that carry the pain signal up to the brain, and inhibitory interneurons that impede transmission cell activity. Activity in both thin and large diameter fibers excites transmission cells. Thin fiber activity impedes the inhibitory cells (tending to allow the transmission cell to fire) and large diameter fiber activity excites the inhibitory cells (tending to inhibit transmission cell activity). So, the more large fiber (touch, pressure, vibration) activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. The authors had drawn a neural "circuit diagram" to explain why we rub a smack. They pictured not only a signal traveling from the site of injury to the inhibitory and transmission cells and up the spinal cord to the brain, but also a signal traveling from the site of injury directly up the cord to the brain (bypassing the inhibitory and transmission cells) where, depending on the state of the brain, it may trigger a signal back down the spinal cord to modulate inhibitory cell activity (and so pain intensity). The theory offered a physiological explanation for the previously observed effect of psychology on pain perception. In 1968, three years after the introduction of the gate control theory, Ronald Melzack concluded that pain is a multidimensional complex with numerous sensory, affective, cognitive, and evaluative components. Melzack's description has been adapted by the International Association for the Study of Pain in a contemporary definition of pain. Although it is now considered to be oversimplified with flaws in the presentation of neural architecture, the gate control theory spurred many studies in pain research and significantly advanced our understanding of pain. == Therapeutic uses ==

The mechanism of gate control theory can be used therapeutically. Gate control theory thus explains how stimulus that activates only nonnociceptive nerves can inhibit pain. The pain seems to be lessened when the area is rubbed because activation of nonnociceptive fibers inhibits the firing of nociceptive ones in the laminae. == See also ==