Iravani M M, Kruk Z L
Department of Pharmacology, Queen Mary and Westfield College, University of London, England.
J Neurochem. 1995 Mar;64(3):1161-8. doi: 10.1046/j.1471-4159.1995.64031161.x.
The effects of (+)-amphetamine on carrier-mediated and electrically stimulated dopamine release were investigated using fast cyclic voltammetry in rat brain slices incorporating the nucleus accumbens, and in the caudate putamen. In the caudate putamen, dopamine release either increased with increasing frequency of local electrical stimulation (hot spots) or did not increase significantly (cold spots); dopamine release increased with increasing frequency of electrical stimulation in the nucleus accumbens. Local pressure application of (+)-amphetamine from a micropipette caused dopamine efflux at all sites examined, and this was not affected by sulpiride, indicating that efflux of dopamine caused by (+)-amphetamine is not regulated by dopamine D2 autoreceptors. (+)-Amphetamine reduced single-pulse electrically stimulated dopamine release at all sites; sulpiride reversed this decrease, indicating that endogenous dopamine released by (+)-amphetamine activates dopamine D2 autoreceptors. In nucleus accumbens and hot spots, (+)-amphetamine did not affect 20-pulse 50-Hz-stimulated dopamine release, whereas in cold spots it potentiated 20-pulse 50-Hz-stimulated dopamine release. We conclude that (+)-amphetamine modifies electrically stimulated dopamine release by uptake inhibition or by indirect activation of D2 autoreceptors; the precise mechanism is determined by site and duration of electrical stimulation.
使用快速循环伏安法，在包含伏隔核的大鼠脑切片以及尾状壳核中，研究了（+）-苯丙胺对载体介导的和电刺激的多巴胺释放的影响。在尾状壳核中，多巴胺释放要么随着局部电刺激频率的增加而增加（热点），要么没有显著增加（冷点）；在伏隔核中，多巴胺释放随着电刺激频率的增加而增加。从微量移液器局部施加（+）-苯丙胺会导致在所检查的所有部位出现多巴胺外流，并且这不受舒必利的影响，表明（+）-苯丙胺引起的多巴胺外流不受多巴胺D2自身受体的调节。（+）-苯丙胺在所有部位均降低单脉冲电刺激的多巴胺释放；舒必利可逆转这种降低，表明（+）-苯丙胺释放的内源性多巴胺激活多巴胺D2自身受体。在伏隔核和热点中，（+）-苯丙胺不影响20脉冲50赫兹刺激的多巴胺释放，而在冷点中它增强20脉冲50赫兹刺激的多巴胺释放。我们得出结论，（+）-苯丙胺通过摄取抑制或通过间接激活D2自身受体来改变电刺激的多巴胺释放；确切机制由电刺激的部位和持续时间决定。
