Zhao X N, Zhang Z X, Shi S L, Wang X G, Yang A Z, Wang T L, Zhao W F, Huang M J, Chen R S
Division of Physiology, Nanjing University, China.
Zhongguo Yao Li Xue Bao. 1990 Mar;11(2):112-6.
After buprenorphine (Bup, 0.8 mg/kg ip) treatment 45Ca-uptake (cpm/mg fresh brain) in vivo by brain slices decreased from 589 +/- 12 and 486 +/- 12 to 522 +/- 14 and 408 +/- 10 and mitochondrial protein bound Tb3+ (Tb3+ relative fluorescent intensity) reduced from 41 +/- 5 and 32 +/- 2 to 30 +/- 3 and 22 +/- 2 in periaqueductal grey and hypothalamus, respectively. A large amount dense precipitate occurred in the myelin sheath and mitochondria in both regions. The 45Ca-uptake evoked by buprenorphine at 16 micrograms/40 microliter in vitro has the similar tendency with that in vivo. Treated by ruthenium red (20 micrograms/mouse ip or icv) before buprenorphine, the above-mentioned effects were all abolished. Similar results were obtained with morphine (Mor, 10 mg/kg ip) and verapamil (Ver, 8 micrograms/mouse icv) instead of buprenorphine and ruthenium red, respectively. These results suggest that Ca2+ transport across neuroplasmic membranes plays a mediator role in drug-induced analgesia.
在丁丙诺啡（Bup，0.8毫克/千克腹腔注射）治疗后，脑切片在体内的45钙摄取量（每毫克新鲜脑的计数/分钟）从589±12和486±12分别降至522±14和408±10，导水管周围灰质和下丘脑中线粒体蛋白结合的Tb3 +（Tb3 +相对荧光强度）分别从41±5和32±2降至30±3和22±2。两个区域的髓鞘和线粒体中均出现大量致密沉淀物。丁丙诺啡在体外16微克/40微升时诱发的45钙摄取与体内情况具有相似趋势。在给予丁丙诺啡之前用钌红（20微克/小鼠腹腔注射或脑室内注射）处理后，上述作用均被消除。分别用吗啡（Mor，10毫克/千克腹腔注射）和维拉帕米（Ver，8微克/小鼠脑室内注射）代替丁丙诺啡和钌红也得到了类似结果。这些结果表明，Ca2 +跨神经细胞质膜的转运在药物诱导的镇痛中起介导作用。
