Lorenzo-Sanz Gustavo, Sánchez-Herranz Antonio
Servicio de Pediatría, Hospital Universitario Ramón y Cajal, Ctra. Colmenar Viejo, Madrid, Spain.
Rev Neurol. 2011 Mar 1;52 Suppl 1:S103-8.
A number of genetic and neuroimagen proofs support the idea that attention-deficit/hyperactivity disorder (ADHD) present a neurobiological alteration. Vesicular monoamine transporters (VMATs) are important proteins that regulate the intraneuronal monoamine concentration and disposition as this protein sequesters cytoplasmic dopamine within synaptic vesicles thus contributing to subsequent excitotoxic release.
Two pharmacologically distinct VMAT isoforms VMAT1 and VMAT2 have been cloned and described. The VMAT2, in the CNS, is responsible for the translocation of dopamine from the cytoplasm into synaptic vesicles. In addition, it has been described a neuroprotector role for these transporters. The platelet vesicular monoamine transporter VMAT2 is used as a peripheral model of neuronal VMAT2. Its quantification has been used to perform studies of ADHD and other neuropsychiatry diseases related with the monoamines metabolism.
Since dopamine and other monoamines (epinephrine and serotonine) play a role in ADHD, and methylphenidate, an usual treatment for this type of patients, modifies the VMAT2 activity, we may argue that VMAT2 is involved in ADHD pathogeny.
大量遗传学和神经影像学证据支持注意缺陷多动障碍（ADHD）存在神经生物学改变这一观点。囊泡单胺转运体（VMATs）是重要的蛋白质，可调节神经元内单胺浓度和分布，因为该蛋白将细胞质多巴胺隔离于突触小泡内，从而促使随后的兴奋性毒性释放。
已克隆并描述了两种药理学特性不同的VMAT亚型VMAT1和VMAT2。在中枢神经系统中，VMAT2负责将多巴胺从细胞质转运至突触小泡。此外，已描述了这些转运体的神经保护作用。血小板囊泡单胺转运体VMAT2用作神经元VMAT2的外周模型。其定量已用于开展ADHD及其他与单胺代谢相关的神经精神疾病的研究。
由于多巴胺和其他单胺（肾上腺素和血清素）在ADHD中起作用，且哌甲酯（这类患者常用的治疗药物）可改变VMAT2活性，我们可以认为VMAT2参与了ADHD的发病机制。
