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Schmerz. 1993 Dec;7(4):216-25.

Descending modulation of spinal nociceptive processing.

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1
Department of Pharmacology, University of Iowa, Bowen Science Building, 52242, Iowa City, IA, USA.

Abstract

The quantitative approach to the study of descending inhibition of spinal nociceptive transmission was initiated in Heidelberg through the use of natural, noxious stimulation and examination of the modulation of the encoding properties of spinal dorsal horn neurons. This important approach required control of the noxious stimulus, which had previously been inadequately considered, and the parametric assessment of modulatory influences on the encoding properties of spinal dorsal horn neurons. As a consequence, descending inhibition of spinal nociceptive transmission was found not to be homogeneous throughout the brainstem, but rather to be significantly different from different brainstem nuclei. The early contributions from Zimmermann's laboratory and subsequent contributions, mostly by previous coworkers, led to a clearer understanding of how these inhibitory systems were organized in the brainstem. For example, it was established in the early 1980s that the nucleus raphe magnus was not the requisite or the only bulbar relay between the midbrain and the spinal cord important to the endogenous pain control system. The same quantitative approach has proved useful in studies of nociceptive reflexes evoked either by noxious thermal or visceral stimuli and in electrophysiological studies of neuronal responses to noxious stimulation of hollow visceral organs. Most recently, the same approach has been profitably applied to studies that have focused onfacilitatory influences descending from many of the same brainstem sites. As a consequence, it has been proposed that there exists an endogenous pain facilitating system analogous to the well-accepted endogenous pain inhibitory system. While the function of the facilitatory system remains unknown, it is proposed that it may be important to long-lasting pain conditions that exist in the absence of pathology.

PMID:
18415386
DOI:
10.1007/BF02529858

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