Mansikka H, Pertovaara A
Department of Physiology, University of Helsinki, Finland.
Brain Res Bull. 1995;37(6):633-8. doi: 10.1016/0361-9230(95)00058-m.
We attempted to find out the role of alpha 2-adrenoceptors of the medullary lateral reticular nucleus (LRN) in antinociception in rats. Spinal antinociception was evaluated using the tail-flick test, and supraspinal antinociception using the hotplate test. Antinociceptive effects were determined following local electric stimulation of the LRN, and following microinjections of medetomidine (an alpha 2-adrenoceptor agonist; 1-10 micrograms), atipamezole (an alpha 2-adrenoceptor antagonist; 20 micrograms) or lidocaine (4%) into the LRN. The experiments were performed using intact and spinalized Hannover-Wistar rats with a unilateral chronic guide cannula. Electric stimulation of the LRN as well as of the periaqueductal gray produced a significant spinal antinociceptive effect in intact rats. Medetomidine (1-10 micrograms), when microinjected into the LRN, produced no significant antinociceptive effect in the tail-flick test in intact rats. However, following spinalization, medetomidine in the LRN (10 micrograms) produced a significant atipamezole-reversible antinociceptive effect in the tail-flick test. In the hot-plate test, medetomidine (10 micrograms) in the LRN produced a significant atipamezole-reversible increase of the paw-lick latency in intact rats. Microinjection of atipamezole (20 micrograms) or lidocaine alone into the LRN produced no significant effects in the tail-flick test. The results are in line with the previous evidence indicating that the LRN and the adjacent ventrolateral medulla is involved in descending inhibition of spinal nocifensive responses. However, alpha 2-adrenoceptors in the LRN do not mediate spinal antinociception but, on the contrary, their activation counteracts antinociception at the spinal cord level.(ABSTRACT TRUNCATED AT 250 WORDS)
我们试图探究延髓外侧网状核(LRN)的α₂ - 肾上腺素能受体在大鼠抗伤害感受中的作用。采用甩尾试验评估脊髓水平的抗伤害感受,采用热板试验评估脊髓以上水平的抗伤害感受。通过对LRN进行局部电刺激,以及向LRN内微量注射美托咪定(一种α₂ - 肾上腺素能受体激动剂;1 - 10微克)、阿替美唑(一种α₂ - 肾上腺素能受体拮抗剂;20微克)或利多卡因(4%)后,确定抗伤害感受效应。实验使用具有单侧慢性引导套管的完整和脊髓横断的汉诺威 - 威斯塔大鼠进行。对LRN以及导水管周围灰质的电刺激在完整大鼠中产生了显著的脊髓抗伤害感受效应。在完整大鼠的甩尾试验中,向LRN内微量注射美托咪定(1 - 10微克)未产生显著的抗伤害感受效应。然而,脊髓横断后,LRN内的美托咪定(10微克)在甩尾试验中产生了显著的、可被阿替美唑逆转的抗伤害感受效应。在热板试验中,LRN内的美托咪定(10微克)在完整大鼠中使舔爪潜伏期显著延长,且可被阿替美唑逆转。单独向LRN内微量注射阿替美唑(20微克)或利多卡因在甩尾试验中未产生显著效应。这些结果与先前的证据一致,表明LRN和相邻的延髓腹外侧参与脊髓伤害性反应的下行抑制。然而,LRN中的α₂ - 肾上腺素能受体并不介导脊髓抗伤害感受,相反,它们的激活在脊髓水平抵消抗伤害感受。(摘要截选至250词)