PAIN AND INFLAMMATION II: CELLULAR AND MOLECULAR MECHANISMS THAT WILL EXERT CHANGES IN THE PERIPHERAL AND CENTRAL NERVOUS SYSTEM

Abstract

 During an inflammatory process, a series of mediators from different origins such as bradikinine, coagulation factors, serotonine, histamine, potassium, ATP, proteinoids, interleukins, neuropeptides, and nerve growth factor, are released. The nociceptors possess receptors for many molecules, and through their interactions they can modify primary neurons activity. They work on this process by the direct activation of these neurons or by reducing their activation threshold, known as peripheral sensitization. clinically, this phenomenon is responsible for the primary hyperalgesia that is present on the injury side. The changes occurred in the activity of the primary neurons added to the modification of their biochemical profile done by the induction of the expression of new proteins, alters spinal synapsis, generating hyperexcitability of the dorsal horn neurons. This phenomenon has been denominated as central sensitization that contributes of pain persistence, even when the tissue is healing. A clinical relation between secondary hyperalgesia and allodinia is present. This article reviews the principal cellular and molecular mechanisms that guide the changes in primary sensory neurons and in the dorsal horn neurons of the spinal cord, in response to an inflammatory process. The knowledgement of these mechanisms has permitted a better understanding of this kind of pain and outlines new treatment approaches for its management.