Abstract
Nerve injury sometimes trigger neuropathic pain states that are exacerbated by sympathetic efferent activity. A classic example is causalgia. The mechanism of coupling between sympathetic efferent activity and the afferent discharge responsible for pain sensation is a subject of controversy. Some authors hold to the direct coupling hypothesis which proposes that noradrenaline (NA), released from sympathetic varicosities, acts directly on alfa-adrenoreceptors located in the membrane of injured primary afferents. Others believe that coupling is indirect: NA released from sympathetic endings, acts back on alfa-adrenoreceptors on the postganglionic terminals themselves, triggering the release of a prostanoid mediator which sensitizes the sensory afferent endings. We report that the responsiveness of injured afferent axons to systemically administered NA persists in rats that underwent prior sympathectomy (n=16). Control group consisted of 16 rats without sympathectomy. The observation of adrenosensitivity in injured afferents in the absence of sympathetic postganglionic endings is consistent with the direct...
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