[Current aspects of nociceptive transmission: peripheral mechanisms and spinal modulation]

Nociceptive transmission shows unusual features of sensorial physiology, due to the complex modulation which occurs from the start of the impulse until its final perception. In recent years the dynamic role played in nociception by peripheral structures, such as the 7 and spinal nociceptors and the second order neurones, has been recognized. It is fairly clear how a number of modulators activate and make nociceptors sensitive, accounting for the appearance of clinical features such as primary hyperalgesia, and their persistance. Thus eico sanoides, histamine, bradykinin and others allow considerable control of nociceptor activity. Also, the dorsal horn neurones play an important part in other clinical signs associated with pain, such as mechanical (secondary) hyperalgesia. At this level, some neurotransmitters such as glutamate or the neurokinins seem to be important in central sensibilization phenomena which occur when a painful stimulus is maintained. In fact, continued release of these neurotransmitters implies the expression of certain genes and the production of certain proteins. Knowledge of the relationship between the different neurochemical systems and subsequent changes in their expression in different pathological situations may help to explain the pathophysiology of some clinical signs of neuropathic pain which are at present inexplicable.