Mechanisms of somatic pain

This article, by the University of Utah pain research center, is very interesting but a little bit too detailed. But is worths reading it once and keeping in mind the  summary points:

1. Somatic pain is normally triggered by the activation of nociceptors. Particular types of nociceptors have been well characterized in cutaneous, articular and muscle nerves.
2. The activation of cutaneous Ad nociceptors causes a sensation of pricking pain, whereas stimulation of C polymodal nociceptors elicits burning pain. Muscle nociceptors produce aching pain.
3. Unlike sensitive mechanoreceptors and thermoreceptors, nociceptors can be sensitized by damaging stimuli. Sensitization appears to be triggered by the release of chemical substances, such as prostaglandins, bradykinin, serotonin, and histamine, into the environment of peripheral nociceptor terminals. Some nociceptors are quite unresponsive until they are sensitized.
4. Nociceptors project to particular laminae in the spinal cord dorsal horn. Cutaneous Ad nociceptive fibers end in laminae I, II, and V, whereas cutaneous C polymodal nociceptors end chiefly in lamina II. Fiber, joint, and muscle afferents project to laminae I and V.
5. Fine afferent terminals, presumably of nociceptors, in the dorsal horn contain peptides, such as substance P and CGRP, and also excitatory amino acids. Both classes of substances are likely to be released during intense noxious stimulation.
6. Noxious stimuli trigger both excitatory and inhibitory events in the dorsal horn. Inhibition is likely to be mediated by such agents as inhibitory amino acids and inhibitory peptides. The circuits may be local or involve a supraspinal loop.
7. STT cells that project to the ventral posterior lateral thalamic nucleus in monkeys and rats have response properties that suit them for a role in the sensory-discriminative aspects of pain. Their input can be from cutaneous, articular, muscle and/or visceral receptors. Convergent inputs may account for pain referral.
8. The responses of STT cells are altered by pathological processes. These neurons become more responsive following damage of the skin by intense mechanical, thermal, or chemical stimuli. A similar change occurs during the development of experimental acute arthritis. It is proposed that sensitization of STT cells helps account for the development of primary and secondary hyperalgesia and allodynia following damage.
9. The mechanism of sensitization of STT cells is likely to involve excitatory amino acid and NK1 receptors.
10. Experimental models of painful neuropathy are being developed by several groups. The responses of STT cells in these models are altered in a fashion consistent with the development of spontaneous pain, allodynia, and hyperalgesia.