Activation of pain transmission nerves
Nerve fibers that transmit pain ("pain nerves") are called Adelta-C
or "capsaicin sensitive". They are very thin and numerous. They
leave the spinal ganglions, where their cellular body is located,
and branch into two extremities:

the peripheral end runs along the nerve root to sensory sites. You
may find these nerve fiber endings in the external part of the disc
fibrous ring as well as in the bone underneath the facet joint. the
central part contacts with a spinal cord cell, which transmits this
sensitivity to the brain.
Pain nerves contain different substances (called "neurotransmitters"
or "neuromodulators"). When nerves are activated they release
these substances. Depending on the extremity and the delivered
substance, the effects may differ. For example: in case of a disc
herniation:

- The nucleus pulposus substances activate the peripheral extremity
of the pain nerves located within the fibrous sheath. When activation
occurs, these ends:
- Send their activation to its central extremity, transmitting
the painful sensation to the spinal cord.
- Release neurotransmitters that essentially contain Substance
P (SP), CGRP and NKA, unleashing neurogenic inflammation
of the herniated disc. From thereon, the herniated material
may increase in volume, compressing the nerve root.
- When the central extremity is activated:
- It initially releases glutamate. Glutamate activates the
spinal cord cell, that:
- Transmits pain to the brain, and the patient begins
to notice pain as of this moment,
- Starts muscle contracture
through a reflex mechanism
- If pain nerve activation lasts longer, substance P is
released and, if released during sufficient time, this neurotransmitter
activates a special receptor at the spinal cord cell. Activation
of this receptor, called the NMDA receptor, conditions cell
structural changes and is responsible for constant activation.
Consequently, if pain persists during sufficient time, it
may remain, although its initial cause may have disappeared.
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