Engstrom R G, Kelly L A, Gogerty J H
Arch Int Pharmacodyn Ther. 1975 Apr;214(2):308-21.
Mazindol, 5-hydroxy-5-(4'-chlorophenyl)-i, 3-dihydro-5H-imidazo-(2, 1-a) isoindole, has demonstrated anorexic activity and other pharmacological responses which suggest alterations in brain norepinephrine metabolism. Studies of the effects of mazindol on neuronal uptake and/or release of norepinephrine showed that mazindol, when given before cerebral intraventricular injection of 3-H-norepinephrine by a mechanism that increases 3-H-normetanephrine synthesis via catechol-O-methyl-transferase and provided no significant effect on deamination of the catecholamine. Studies designed to measure norepinephrine release showed that mazindol (in contrast to d-amphetamine) did not cause release of 3-H-norepinephrine from neuronal stores. Furthermore, mazindol did not inhibit norepinephrine synthesis, whereas d-amphetamine did. The effect of d-amphetamine on norepinephrine release and synthesis may be more important than effects on uptake of this catecholamine. In contrast, mazindol appears to produce its primary effect on norepinephrine metabolism by inhibition of neuronal uptake mechanism.
马吲哚，即5-羟基-5-(4'-氯苯基)-1,3-二氢-5H-咪唑并-(2,1-a)异吲哚，已显示出厌食活性和其他药理反应，提示脑去甲肾上腺素代谢发生改变。关于马吲哚对去甲肾上腺素神经元摄取和/或释放影响的研究表明，在脑室内注射3-H-去甲肾上腺素之前给予马吲哚，其机制是通过儿茶酚-O-甲基转移酶增加3-H-去甲变肾上腺素的合成，且对儿茶酚胺的脱氨基作用无显著影响。旨在测量去甲肾上腺素释放的研究表明，马吲哚（与右旋苯丙胺不同）不会导致神经元储存的3-H-去甲肾上腺素释放。此外，马吲哚不抑制去甲肾上腺素的合成，而右旋苯丙胺会抑制。右旋苯丙胺对去甲肾上腺素释放和合成的作用可能比其对这种儿茶酚胺摄取的作用更重要。相比之下，马吲哚似乎主要通过抑制神经元摄取机制对去甲肾上腺素代谢产生作用。
