• W Jänig, J D Levine, and M Michaelis.
• Physiologisches Institut, Christian-Albrechts-Universitat zu Kiel, Germany. w.janig@physiologie.uni-kiel.de
• Prog. Brain Res. 1996 Jan 1; 113: 161-84.

AbstractSympathetic post-ganglionic neurons may be involved in the generation of pain, hyperalgesia and inflammation under pathophysiological conditions. Two categories of influence of the sympathetic neuron on afferent neurons can be distinguished and this distinction seems to be related to whether the coupling between afferent and sympathetic neuron develops after nerve lesion or after tissue trauma with inflammation (Fig. 15): A. Peripheral nerve lesion generates plastic changes of the afferent and sympathetic postganglionic neurons, depending on the type of nerve lesion (e.g. complete, partial). Both afferent and post-ganglionic neurons exhibit degenerative and regenerative changes and unlesioned neurons may show collateral sprouting in the periphery as well as in the dorsal root ganglion. This reorganization of the peripheral neurons may lead to chemical coupling between sympathetic and afferent neurons. The coupling is responsible for sensitization and/or activation of primary afferent neurons by the sympathetic neurons. The mediator probably is norepinephrine, but other substances cannot be excluded. The afferent neuron expresses or upregulates functional adrenoceptors. The type of adrenoceptor involved is probably alpha 2. The coupling may occur at different sites of the primary afferent neuron, e.g. at the lesion site, remote from the lesion site in the dorsal root ganglion or between nonlesioned sympathetic and afferent neurons which show collateral sprouting. The biochemical signals which trigger these changes probably are neurotrophic substances, their receptors which are synthesized by the peripheral neurons, Schwann cells and other cells in response to the peripheral lesions. B. Sympathetic nerve terminals in peripheral tissues may serve as mediator elements in hyperalgesia and inflammation following tissue trauma without nerve lesion. Experiments show that these functions are largely independent of activity in the sympathetic neurons and independent of vesicular release of transmitter substances (such as norepinephrine). Sensitization of nociceptive afferents for mechanical stimuli and venular plasma extravasation in the synovium which are induced by the inflammatory mediator bradykinin are, at least in part, dependent on the sympathetic terminal. The signal to venules and afferent receptors is synthesized and released from the sympathetic terminal or in association with it. It is a prostaglandin (probably PGE2). Sympathetically mediated (neurogenic) inflammation and neurogenic inflammation mediated by afferents may interact reciprocally and enhance the inflammatory process as well as the sensitization of nociceptive afferents. Norepinephrine may also lead to sensitization of nociceptive afferents under inflammatory conditions. This sensitization is presumably mediated by alpha 2-adrenoceptors in the sympathetic varicosities and by a prostaglandin (probably PGI2) which is synthesized and released by or in association with the sympathetic varicosities.

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