Huang J T, Wajda I J
Br J Pharmacol. 1977 Jul;60(3):363-7. doi: 10.1111/j.1476-5381.1977.tb07509.x.
1 Choroid plexus obtained from the lateral ventricles of the rat actively accumulated homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). 2 Morphine 5 X 10(-6) M to 5 X 10(-4)M potentiated 5-HIAA accumulation but did not affect HVA accumulation. Levorphanol and dextorphan had little effect. 3 Naloxone at high concentrations inhibited both HVA and 5-HIAA accumulation. 4 Glutamic acid, glycine, and arginine also decreased 5-HIAA accumulation, but lysine, tryptophan, and aspartic acid had no effect. 5 Probenecid, naloxone, arginine, glycine, and tryptophan blocked the increase of 5-HIAA accumulation induced by morphine. 6 Acute or chronic morphine treatment did not increase the accumulation of 5-HIAA. 7 These results suggest that the increase of 5-HIAA or HVA in brain by morphine is not due to the inhibition of the elimination of these metabolites from the choroid plexus.
1 从大鼠侧脑室获取的脉络丛能主动摄取高香草酸(HVA)和5-羟吲哚乙酸(5-HIAA)。2 浓度为5×10⁻⁶M至5×10⁻⁴M的吗啡能增强5-HIAA的摄取,但不影响HVA的摄取。左啡诺和右啡烷作用甚微。3 高浓度的纳洛酮能抑制HVA和5-HIAA的摄取。4 谷氨酸、甘氨酸和精氨酸也能降低5-HIAA的摄取,但赖氨酸、色氨酸和天冬氨酸则无此作用。5 丙磺舒、纳洛酮、精氨酸、甘氨酸和色氨酸能阻断吗啡诱导的5-HIAA摄取增加。6 急性或慢性吗啡处理并未增加5-HIAA的摄取。7 这些结果表明,吗啡导致脑内5-HIAA或HVA增加并非由于抑制了这些代谢产物从脉络丛的清除。