The They influence the degree of nerve activity

The process of nociception
explains how the body processes pain, and it begins when a stimulus stimulates
nociceptors, which are highly specialised primary sensory neurones found
primarily in the skin, joints or organs such as the liver. The classification of nociceptors
can be derived into two categories; lightly myelinated A? fibers and unmyelinated C fibers
and due to their difference in conduction velocity, the action potential of the
A? fibers can travel at a rate of
around 20m/s, whereas the C fibres conduct at slower speeds of around 2m/s
(Fein 2014). C-fiber nociceptors respond poly-modally to thermal, mechanical,
and chemical stimuli; and the A?-fiber nociceptors are of two types and respond
to mechanical and mechano-thermal stimuli (Patel 2010). (Lamont et al, 2000) explain
how A-fiber nociceptors are responsible for signaling ‘first pain,’ which can
be described as a ‘sharp, stinging, or pricking sensation’, it is also ‘localized
and transient, lasting only as long as the acute painful stimulus is activating
the nociceptor’. In contrast, Lamont et al also explain that if a stimulus is
of sufficient magnitude, C-fiber nociceptors are recruited and mediate ‘slow
pain,’ which is ‘a more diffuse and persistent burning sensation extending
beyond the termination of an acute painful stimulus’.

The first stage
of nociception is transduction, and is modulated by a number of chemical
substances produced when the cell is damaged. They influence the degree of
nerve activity and hence intensity of the pain sensation. The chemical
mediators released from the damaged cell include prostaglandin, serotonin which
is released from platelets and histamine released from mast cells (Patel 2010).
The release of histamine as well as substance P causes vasodilation, a
protective mechanism which eventually promotes healing and protection against
infection. An action potential is generated due to the presence of ion channels
which are tuned to respond with a high threshold only to particular features of the
mechanical, thermal, and chemical environment (Ramsey et al, 2006). When the
channels are activated, depolarization of the membrane occurs due to voltage
voltage-dependent sodium and potassium channels and potassium ions.

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The next stage is the transmission of pain, where the impulse
travels along the nociceptor axons to their cell bodies located in the dorsal
root ganglion in the spinal cord, and then to their central terminals in the
dorsal horn, which is organized into different laminae. Lamina II is also known as the
substantia gelatinosa and this extends from the trigeminal nucleus in the
medulla, to the filum terminale at the caudal end of the spinal cord. (Steeds,
2016). Most nociceptive A?- and C-fibres terminate superficially in laminae
I–II, with a smaller number reaching deeper laminae (Dickinson, 2008). Projection
neurons in the dorsal horn relay nociceptive inputs to higher centers in the
brain via five major ascending pathways, the main ascending
pathway being the spinothalamic tract located in the anterolateral white
matter of the spinal cord. Axons travelling in the lateral and medial spinothalamic
tracts terminate in their respective medial and lateral nuclei and from here
neurons project to the primary and secondary somatosensory cortices, the
insula, the anterior cingulate cortex and the prefrontal cortex, and these
areas are involved in the perception of pain.

Finally, the modulation of pain
involves changing or inhibiting transmission of pain impulses in the spinal
cord. Excitatory neuropeptides including glutamate, aspartate and
substance P can facilitate and amplify the pain signals in ascending projection
neurons. Similarly, endogenous (opioid, serotonergic and noradrenergic)
descending analgesic systems serve to dampen the nociceptive response. Two important areas of the
brainstem are involved in reducing pain: the periaquaductal grey (PAG) and the
nucleus raphe magnus (NRM), PAG (anti-nociceptor) neurons excite cells in the
NRM that in turn project down to the spinal cord to block pain transmission by
dorsal horn cells. Stimulation of the raphe nuclei produces a powerful
analgesia and it is thought that the serotonin released by this stimulation
activates inhibitory interneurons even more powerfully than noradrenaline and
thus blocks pain transmission