Carlsson S G, Ahlenius S
Scand J Psychol. 1977;18(2):157-60. doi: 10.1111/j.1467-9450.1977.tb00271.x.
The administration of d-amphetamine sulphate resulted in a restoration of intracranial self-stimulation (ICSS) suppressed by tetrabenazine (TBZ). A dose-dependent increase in the rate of ICSS was seen after L-dopa in animals pretreated with TBZ. d-Amhetamine is believed to act by facilitating the nerve-impulse induced release of central catecholamines (CA) whereas the blockage of the granular uptake-storage mechanism by TBZ will prevent the storage of CA formed from the administrated L-dopa and thereby interfere with their release by nerve-impulses. Thus, in the latter case, an activation of central CA receptors in all probability will be due to a dose-dependent diffusion of CA from nerve terminals. It is suggested that the failure to completely antagonize the TBZ-induced suppression of behaviour by L-dopa is due to the fact that a direct activation, independent of the nerve-impulse flow, of central CA receptors easily results in an overstimulation and a reduced specificity in behaviour.
给予硫酸右旋苯丙胺可使被丁苯那嗪（TBZ）抑制的颅内自我刺激（ICSS）恢复。在经TBZ预处理的动物中，左旋多巴给药后ICSS速率呈剂量依赖性增加。据信，右旋苯丙胺的作用是促进神经冲动诱导的中枢儿茶酚胺（CA）释放，而TBZ对颗粒摄取-储存机制的阻断会阻止由给药的左旋多巴形成的CA的储存，从而干扰其通过神经冲动的释放。因此，在后一种情况下，中枢CA受体的激活很可能是由于CA从神经末梢的剂量依赖性扩散。有人提出，左旋多巴未能完全拮抗TBZ诱导的行为抑制，是因为中枢CA受体的直接激活（独立于神经冲动流）很容易导致过度刺激和行为特异性降低。
