The Gate Control Theory

The Gate Control Theory

Acupuncture is also thought to work through the “Gate Control” theory of pain. This theory presented by Patrick Wall and Ronald Melzack in 1965, states that pain is a function of the balance between messages in the central nervous system (brain and spinal cord) and the peripheral nervous system (branching nerves within the body). In essence the theory is about how many messages the body can carry and listen and respond to at one time. By stimulating the large nerve fibers (as acupuncture appears to do) you can essentially block the bodies ability to experience “pain”. As with the endorphin theory, this theory does not explain acupunctures effect on other chemistry and other non-pain related conditions. Nor does it explain why the effects of acupuncture can last for significant periods of time following a treatment.

When you experience a negative feeling, 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.[citation needed] 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.[citation needed] However, activation of the inhibitory interneurons varies: large-diameter fibers excite the interneuron, which ultimately reduces transmission cell firing[citation needed], 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.[citation needed]

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.[4] The nonnociceptive fibers indirectly inhibit the effects of the pain fibers, ‘closing a gate‘ to the transmission of their stimuli.[4] In other parts of the laminae, pain fibers also inhibit the effects of nonnociceptive fibers, ‘opening the gate’.[4] This presynaptic inhibition of the dorsal nerve endings can occur through specific types of GABAA receptors (not through the α1 GABAA receptor and not through the activation of glycine receptors which are also absent from these types of terminals). Thus certain GABAA receptor subtypes but not glycine receptors can presynaptically regulate nociception and pain transmission.

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.[4] 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.[4]