Ohta Y, Alojado M E, Kemmotsu O
Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, Sapporo, Japan.
Anesth Analg. 1995 May;80(5):890-5. doi: 10.1097/00000539-199505000-00007.
The nucleus raphe magnus (NRM) is an important descending pain inhibitory system. We postulated that the analgesic action of supraspinally administered opiates results from increased descending inhibitory control of the NRM. We tested whether fentanyl activates NRM neurons in the rat slice preparation using extra-cellular recording. Eighty-seven percent of NRM neurons (total number = 68) tested were spontaneously active with firing frequencies of 0.2-4 spikes/s in artificial cerebrospinal fluid. Application of fentanyl (0.25, 0.5, and 1 mumol/L) increased firing frequencies in 12 of 59 (20%) spontaneously active neurons. In 6 of 9 (67%) silent neurons, fentanyl induced firing activities. Naloxone (1-2 mumol/L) antagonized the increased or induced activities by fentanyl in three neurons. In 13 of 59 (22%) spontaneously active neurons, fentanyl decreased the firing frequencies. Although fentanyl was associated with increased activity in a total of 18 NRM neurons, fentanyl at a higher concentration significantly increased the number of inhibited neurons. The results indicate that fentanyl partly activates the descending inhibitory system originating from the NRM; however, at higher concentrations, it appears also to inhibit this same system.
中缝大核（NRM）是重要的下行性疼痛抑制系统。我们推测脊髓上给予阿片类药物的镇痛作用源于中缝大核下行抑制控制的增强。我们使用细胞外记录法，在大鼠脑片制备中检测芬太尼是否激活中缝大核神经元。在人工脑脊液中，所检测的68个中缝大核神经元中有87%（总数）具有自发放电活动，放电频率为0.2 - 4次/秒。应用芬太尼（0.25、0.5和1μmol/L）使59个自发放电神经元中的12个（20%）放电频率增加。在9个静息神经元中的6个（67%），芬太尼诱导出放电活动。纳洛酮（1 - 2μmol/L）拮抗了芬太尼在3个神经元中引起的放电频率增加或诱导出的放电活动。在59个自发放电神经元中的13个（22%），芬太尼降低了放电频率。虽然芬太尼使总共18个中缝大核神经元的活动增加，但较高浓度的芬太尼显著增加了被抑制神经元的数量。结果表明，芬太尼部分激活了起源于中缝大核的下行抑制系统；然而，在较高浓度时，它似乎也抑制这个相同的系统。
