Kalivas Peter W
Department of Neurosciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Dialogues Clin Neurosci. 2007;9(4):389-97. doi: 10.31887/DCNS.2007.9.4/pkalivas.
Although the pharmacology of amphetamine-like psychostimulants at dopamine transporters is well understood, addiction to this class of drugs has proven difficult to deal with. The reason for this disconnection is that while the molecular mechanism of amphetamine action is critical to reinforce drug use, it is only the first step in a sequence of widespread neuroplastic events in brain circuitry. This review outlines the affect of psychostimulants on mesocorticolimbic dopamine projections that mediate their reinforcing effect, and how this action ultimately leads to enduring pathological neuroplasticity in glutamatergic projections from the prefrontal cortex to the nucleus accumbens. Molecular neuroadaptations induced by psychostimulant abuse are described in glutamate neurotransmission, and from this information potential pharmacotherapeutic targets are identified, based upon reversing or countermanding psychostimulant-induced neuroplasticity.
尽管苯丙胺类精神兴奋剂对多巴胺转运体的药理作用已为人熟知,但事实证明,对这类药物的成瘾问题很难处理。这种脱节的原因在于,虽然苯丙胺作用的分子机制对于强化药物使用至关重要,但它只是大脑回路中一系列广泛的神经可塑性事件的第一步。本综述概述了精神兴奋剂对介导其强化作用的中脑边缘多巴胺投射的影响,以及这种作用最终如何导致从前额叶皮质到伏隔核的谷氨酸能投射中持久的病理性神经可塑性。文中描述了精神兴奋剂滥用所诱导的分子神经适应性变化在谷氨酸神经传递中的情况,并基于逆转或对抗精神兴奋剂诱导的神经可塑性,从这些信息中确定了潜在的药物治疗靶点。