Almeida A, Tjølsen A, Lima D, Coimbra A, Hole K
Institute of Histology and Embryology, University of Oporto, Portugal.
Brain Res Bull. 1996;39(1):7-15. doi: 10.1016/0361-9230(95)02027-6.
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 hot-plate tests. Lesions of the DRt were obtained by injecting quinolinic acid (180 nmol/microliters) unilaterally or bilaterally, and nociceptive responses were evaluated by both tests. Following unilateral lesions, the tail-flick latencies and the hot-plate response temperatures were increased, values differing statistically from controls in the latter test. Bilateral lesions resulted in statistically significant increases of both tail-flick latency and hot-plate response temperature. Stimulation of the DRt was performed by injecting glutamate (100 nmol/microliters) 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 involved in the facilitation of nociception after acute thermal noxious stimulation. This effect may be mediated through a spino-DRt-spinal loop causing a rebound of excitation in lamina I cells receiving noxious input from their own receptive field.
利用甩尾试验和渐增温度热板试验,研究了损毁或刺激延髓背侧网状核(DRt)对痛觉处理的影响。通过单侧或双侧注射喹啉酸(180纳摩尔/微升)造成DRt损伤,并通过这两种试验评估伤害性反应。单侧损伤后,甩尾潜伏期和热板反应温度增加,在热板试验中,这些值与对照组相比有统计学差异。双侧损伤导致甩尾潜伏期和热板反应温度均有统计学意义的增加。通过单侧注射谷氨酸(100纳摩尔/微升)刺激DRt,与注射生理盐水的对照组相比,1分钟后甩尾潜伏期显著缩短。这些结果表明,DRt参与急性热损伤刺激后痛觉的易化。这种效应可能通过脊髓-DRt-脊髓环路介导,导致接受来自其自身感受野伤害性输入的I层细胞兴奋反弹。