Send to

Choose Destination
Neuroscience. 1995 Dec;69(3):931-8.

The spinal transmission of nociceptive information: modulation by the caudal medulla.

Author information

INSERM U-161, Paris, France.


Multiple descending systems for pain control originate from the rostral medulla and midbrain. These systems are involved in the antinociceptive action produced by opioids. One category of descending inhibitory controls is activated specifically by noxious stimuli and has been termed diffuse noxious inhibitory controls. These controls have been described in both animal and man, but their supraspinal circuitry has not been fully localized. To determine the supraspinal level of integration of nociceptor activated controls and hence their potential relationships with previously described descending controls, we studied in halothane-anesthetized rats the effects of transections performed at various levels in the brainstem. The physiological properties of dorsal horn convergent neurons, including supraspinally-mediated inhibitory processes elicited by heterotopic noxious stimuli, i.e. diffuse noxious inhibitory controls, were not altered in rats in which the brainstem had been completely transected up to 200 microns caudal to the caudal end of the rostral ventromedial medulla. In contrast, the spontaneous activity of these neurons was significantly enhanced and the inhibitory phenomena significantly reduced in animals with transections more than 500 microns caudal to the caudal end of the rostral ventromedial medulla. These effects were not related to cardiovascular changes induced by the transections. These data indicate that some tonic descending inhibitory controls and diffuse noxious inhibitory controls depend upon connections in the caudal medulla. It is proposed that this area constitutes another level from which the transmission of nociceptive information can be modulated and that it acts co-operatively with previously described modulatory systems in the spinal cord and at more rostral levels of the brainstem.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center