Wise R A, Rompre P P
Department of Psychology, Concordia University, Montreal, Canada.
Annu Rev Psychol. 1989;40:191-225. doi: 10.1146/annurev.ps.40.020189.001203.
While the evidence is strong that dopamine plays some fundamental and special role in the rewarding effects of brain stimulation, psychomotor stimulants, opiates, and food, the exact nature of that role is not clear. One thing is clear: Dopamine is not the only reward transmitter, and dopaminergic neurons are not the final common path for all rewards. Dopamine antagonists and lesions of the dopamine systems appear to spare the rewarding effects of nucleus accumbens and frontal cortex brain stimulation (Simon et al 1979) and certainly spare the rewarding effects of apomorphine (Roberts & Vickers 1988). It is clear that reward circuitry is multisynaptic, and since dopamine cells do not send axons to each other or receive axons from each other, dopamine can at best serve as but a single link in this circuitry. If dopamine is not a final common path for all rewards, could it be an intermediate common path for most rewards? Some workers have argued against such a view, but at present they must do so on incomplete evidence. For example, Phillips (1984) has argued that there must be multiple reward systems, functionally independent and organized in parallel with one another. His primary evidence, however, is the fact that brain stimulation is rewarding at different levels of the nervous system. As we have seen in the case of midline mesencephalic stimulation, the location of the electrode tip in relation to the dopamine cells and fibers tells us little about the role of dopamine in brain stimulation reward. It seems clear that the ventral tegmental dopamine system plays a critical role in midline mesencephalic reward, despite the distance from the electrode tip to the dopamine cells where morphine causes its dopamine-dependent facilitory effects or to the dopamine terminals where low-dose neuroleptics presumably cause theirs. Until pharmacological challenge has been extended to the cases discussed by Phillips, we can only speculate as to the role of dopamine in each of those cases. In the cases where pharmacological challenge has been examined, only nucleus accumbens and frontal cortex have been found to have dopamine-independent reward sites. It is not consistent with the dopamine hypothesis that dopamine-independent reward sites should exist in these areas, since any reward signals carried to nucleus accumbens or frontal cortex by dopamine fibers would-unless we are to believe that reward "happens" at these sites-have to be carried to the next stage of the circuit by nondopaminergic fibers (there are no dopaminergic cell bodies in any of the dopamine terminal areas).(ABSTRACT TRUNCATED AT 400 WORDS)
虽然有充分证据表明多巴胺在脑刺激、精神运动兴奋剂、阿片类药物和食物的奖赏效应中发挥着某些基本且特殊的作用,但其作用的确切性质尚不清楚。有一点是明确的:多巴胺并非唯一的奖赏递质,多巴胺能神经元也不是所有奖赏的最终共同通路。多巴胺拮抗剂和多巴胺系统损伤似乎并未消除伏隔核和额叶皮质脑刺激的奖赏效应(西蒙等人,1979年),当然也未消除阿扑吗啡的奖赏效应(罗伯茨和维克斯,1988年)。显然,奖赏回路是多突触的,而且由于多巴胺细胞之间既不相互发送轴突,也不相互接收轴突,多巴胺充其量只能作为该回路中的一个单一环节。如果多巴胺不是所有奖赏的最终共同通路,那么它会是大多数奖赏的中间共同通路吗?一些研究人员反对这种观点,但目前他们只能基于不完整的证据来这样做。例如,菲利普斯(1984年)认为必然存在多个奖赏系统,它们在功能上相互独立且彼此并行组织。然而,他的主要证据是脑刺激在神经系统的不同水平上都具有奖赏作用这一事实。正如我们在中脑中线刺激的例子中所看到的,电极尖端相对于多巴胺细胞和纤维的位置,对于多巴胺在脑刺激奖赏中的作用几乎没有告诉我们什么。很明显,腹侧被盖区多巴胺系统在中脑中线奖赏中起着关键作用,尽管从电极尖端到吗啡产生其多巴胺依赖性促进作用的多巴胺细胞,或者到低剂量抗精神病药物可能产生作用的多巴胺终末,距离都很远。在药理学挑战扩展到菲利普斯所讨论的情况之前,我们只能推测多巴胺在每种情况下的作用。在已经研究过药理学挑战的情况下,仅发现伏隔核和额叶皮质存在不依赖多巴胺的奖赏位点。多巴胺非依赖性奖赏位点存在于这些区域,这与多巴胺假说不一致,因为多巴胺纤维携带到伏隔核或额叶皮质的任何奖赏信号——除非我们相信奖赏“发生”在这些位点——都必须由非多巴胺能纤维传递到回路的下一阶段(在任何多巴胺终末区域都没有多巴胺能细胞体)。(摘要截取自400字)