This is the behavioral correlate of the gated neural control of nociception. It requires an understanding of the anatomy, biology, physiology, and psychology of how we perceive a stimulus as pain.
What is important here is to understand that nociception is the stimulus that initially begins the peripheral nervous system (PNS) sensory pathway to the central nervous system (CNS) spinal cord, causing our brain to interpret a stimulus as pain. Nociceptors are receptors of sensory fibers (specialized axons) which have their cell bodies in groups of neurons called ganglia. The two most important types of axons in this pathway are the Aβ axons and the C axons.
Aβ fibers are large diameter, fast myelinated nociceptive axons which are activated by touch, pressure, and vibration. C fibers are small diameter, slow unmyelinated nociceptive axons which are activated by temperature, pain, and itch.
The sensory dorsal horn of the spinal cord is arranged in laminae that contain local inhibitory GABAergic interneurons that synapse on glutamatergic projection neurons. The projection neurons generally begin the spinothalamic pathway to the brain.
The key applied concept to understand is that Aβ fibers have excitatory synapses on both the inhibitory interneurons and projection neurons vs C fibers have inhibitory synapses on the inhibitory interneurons and excitatory synapses on the projection neurons. Inhibiting the inhibitory interneurons is called disinhibition.
Admittedly, stubbing your toe elicits a sudden touch/pressure stimulus on your toe, activating nociceptors of the Aβ and C fibers. Because Aβ fibers are myelinated and fast, their action potentials very quickly travel to the spinal cord dorsal horn, activating first the inhibitory interneurons which inhibit the projection neurons. This fast inhibition of the projection neurons is why our sense of pain is initially delayed. But as activity continues along the Aβ fiber, the projection neurons are activated. Concurrently, action potentials along the C fibers are relatively slow and when reaching the inhibitory interneurons, the C fibers inhibit the interneurons, thus disinhibiting the projection neurons. At the same time, the C fibers further activate the already disinhibited and Aβ activated projection neurons. It is this disinhibition of interneurons and double activation of the projection neurons that opens the gate in activating the spinothalamic pathways to the brain.
We should also now be able to understand why applying pressure to our stubbed toe by immediately rubbing it often lessens our sensation of pain in stimulating the Aβ nociceptors.
In summary, the Aβ and C fibers are in fact not part of a pain pathway per se, but a nociceptive pathway. The spinothalamic tract to the thalamus is where nociception is eventually coded into pain and depends on what is called our limbic valence, the threshold for what we consider painful. The thalamocortical pathway ends the nociceptive path to the brain cortex where nociception is further interpreted into pain or suffering.
So, what we have here is the structure/function correlate of an elegantly constructed, gated neural pathway that describes nociception, pain, and suffering…
-jq
