The influence on pain processing caused by destruction or stimulation
of the dorsal reticular nucleus (DRt) was studied using the tail-flick
and the increasing temperature hotplate tests. Lesions of the DRt wer
e obtained by injecting quinolinic acid (180 nmol/mu l) unilaterally o
r bilaterally, and nociceptive responses were evaluated by both tests.
Following unilateral lesions, the tail-flick latencies and the hot-pl
ate response temperatures were increased, values differing statistical
ly from controls in the latter test. Bilateral lesions resulted in sta
tistically significant increases of both tail-flick latency and hot-pl
ate response temperature. Stimulation of the DRt was performed by inje
cting glutamate (100 nmol/mu l) unilaterally, which was followed 1 min
later by a significant decrease in the tail-flick latency compared to
saline injected controls. These results suggest that the DRt is invol
ved in the facilitation of nociception after acute thermal noxious sti
mulation. This effect may be mediated through a spino-DRt-spinal loop
causing a rebound of excitation in lamina I cells receiving noxious in
put from their own receptive field.