Gate control theory of pain: Encyclopedia II - Gate control theory of pain - Physiology

Gate control theory of pain - Physiology

Afferent pain-receptive nerves, those that bring signals to the brain, comprise at least two kinds of fibers - a fast, relatively thick, myelinated "Aδ" fiber that carries messages quickly with intense pain, and a small, unmyelinated, slow "C" fiber that carries the longer-term throbbing and chronic pain. Large-diameter Aβ fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibers.

The central 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 (Kandel et al., 2000). The nonnociceptive fibers indirectly inhibit the effects of the pain fibers, 'closing a gate' to the transmission of their stimuli (Kandel et al., 2000). In other parts of the laminae, pain fibers also inhibit the effects of nonnociceptive fibers, 'opening the gate'.

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. The C fiber's synapse would inhibit the inhibitory interneuron, indirectly increasing the projection neuron's chance of firing. The Aβ fiber, on the otherhand, 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 (Kandel et al., 2000).

Gate control theory thus explains how stimulus that activates only nonnociceptive nerves (such as rubbing a bumped knee) 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 (Kandel et al., 2000). In transcutaneous electrical stimulation (TENS), nonnociceptive fibers are selectively stimulated with electrodes in order to produce this effect and thereby lessen pain.

One area of the brain involved in reduction of pain sensation is the periaqueductal gray matter that surrounds the third ventricle and the cerebral aqueduct of the ventricular system. Stimulation of this area produces analgesia (but not total numbing) by activating descending pathways that directly and indirectly inhibit nocicpetors in the laminae of the spinal cord (Kandel et al., 2000). It also activates opioid receptor-containing parts of the spinal cord.

Afferent pathways interfere with each other constructively, so that the brain can control the degree of pain that is perceived, based on which pain stimuli are to be ignored to pursue potential gains. The brain determines which stimuli are profitable to ignore over time. Thus, the brain controls the perception of pain quite directly, and can be "trained" to turn off forms of pain that are not "useful". This understanding led Melzack to point out that pain is in the brain.

Adapted from the Wikipedia article "Physiology", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki