Spinal anti-nociception

Mechanisms to reduce nociceptor input operate at both the spinal and supraspinal level. At the spinal cord level, whether a stimulus is perceived as painful or not depends on the relative activity of large and small diameter fibers. High large/small diameter fiber activity reduces nociceptor input. A modern version of this gate control theory circuitry is shown in figure

Wide dynamic range neurons in lamina V get convergent excitatory input from large (Aβ) mechanoreceptor afferents and small (Aδ and C) nociceptor afferents. The Aβ fibers inhibit lamina V neurons via inhibitory interneurons in lamina II. The nociceptor afferents also excite the lamina V cells by way of excitatory interneurons, and these can be inhibited by the Aβ-driven inhibitory interneurons. Hence, nociceptor afferents excite the lamina V cells both directly and via excitatory interneurons. However, large diameter afferent activity reduces nociceptor input to lamina V cells by increasing inhibition from the lamina II interneurons. Therefore co-activation of low and high threshold afferents closes the pain gate.

The gate control theory accounts for counter-stimulation analgesia in which pain is reduced by stimulating low threshold afferents; we instinctively rub the site of a painful blow, stimulating the mechanoreceptors. Transcutaneous electrical nerve stimulation (TENS) delivers high frequency, low intensity currents, adequate to stimulate Aβ fibers, and also Aδ fibers that activate endogenous opioid-using supraspinal anti-nociception pathways. It is used mainly during childbirth and physiotherapy.