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PAIN Somatic sensation also depends on nociceptors (unmyelinated) that signal that body tissue is being damaged or is at risk of being damaged. The information from nociceptors takes a path to the brain that is largely distict from the path taken by mechanoreceptors. Selective activation of nociceptors can lead to the conscious experience of pain. Nociception and pain are not the same thing. Pain is the feeling or the pereception of irritating, sore, stinging, and unbearable sensations arising from a party of the body. Nociception is the sensory process that provides the signals that trigger pain. Nociceptors and the Transduction of Painful Stimuli Nociceptors are activated by stimuli that have the potential to cause tissue damage. Examples are: strong mechanical stimulation, extremes in temperature, oxygen deprivation, and exposure to certain chemicals. The membranes of nociceptors contain ion channels that are activated by these stimuli. Types of Nociceptors The transduction of painful stimuli occurs in the free nerve endings of unmyelinated C fibers and lightly myelinated Aδ fibers. The majority of nociceptors respond to mechanical, thermal, and chemical stimuli. They are called polymodal nociceptors. Other nociceptors show selectivity in their responses to different stimuli.  Mechanical nociceptors: sensitive to strong pressure  Thermal nociceptors: sensitive to burning heat or extreme cold Chemical nociceptors: show selective responses to histamine and other chemicals Nociceptors are present in most body tissues and are notably abset in the brain (except for the meninges). Hyperalgesia Nociceptors normally respond only when stimuli are strong enough to damage tissue. However, skin, joints, or muscles that have already been damaged or inflammed are unusually sensitive. This is known as hyperalgesia and it is the most familiar example of our body’s ability to control its own pain.  Hyperalgesia can be a reduced threshold for pain, an increased intensity of painful stimuli, or even spontaneous pain.  Primary hyperalgesia occurs within the area of damaged tissue.  Tissues surrounding damaged area may become supersensitive as well by the process of secondary hyperalgesia. Many different mechanisms appear to be invovled in hyperalgesia. A number of these chemcials modulate the excitability of nociceptors, making them more sensitive to thermal or mechanical stimuli. Some examples are: bradykinin, prostaglandins, and substance P (see Fig. 12.24).  Bradykinin directly depolarizes nociceptors and stimulates long-lasting intracellular changes that make heat-activated ion channels more sensitive.  Prostaglandins are generated by the enzymatic breakdown of lipid membrane. They increase the sensitivity of nocireceptors to other stimuli. o Aspirin inhibits the enzymes required for prostaglandin synthesis  Susbstance P synthesized by the nocireceptors themselves. Activation of one branch of a nociceptor axon can lead to the secretion of substance P by other branches of that axon in the neighbouring skin. Substance P causes vasodilation and release of histamine from mast cells. o Sensitization of other nociceptors around the site of injury by substance P is one cause of secondary hyperalgesia. CNS mechanisms also contribute to secondary hyperalgesia. Following injury, the activation of mechanoreceptive Aβ axons by light touch can evoke pain. Primary Afferents and Spinal Mechanisms Aδ and C fibers bring information to the CNS at different rates. Activation of skin nociceptors produces two distinct perceptions of pain:  A fast and sharp first pain, followed by a duller, longer-lasting second pain  First pain is caused by the activation of Aδ fibers whilst second pain is cauesd by the activation of C fibers (see Fig. 12.25). Like the Aβ mechanosensory fibers, the small-diameter fibers have their cell bodies in the segmental dorsal root ganglia and enter the dorsal horn of the spinal cord. These fibers then branch and travel a short distance up and down a region of the spinal cord called the zone of Lissauer. Finally, the fibers synapse on the substantia gelatinosa (see Fig. 12.26). The neurotransmitter of pain afferents is believed to be glutamate. These neurons al
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