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Involvement of vesicular monoamine transporter in attention deficit hyperactivity disorder

G. Lorenzo-Sanz, A. Sánchez-Herranz [REV NEUROL 2011;52 (Supl. 1):S103-S108] PMID: 21365590 DOI: https://doi.org/10.33588/rn.52S01.2011058

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Volumen 52 | Number S01 | Nº of views of the article 21.964 | Nº of PDF downloads 781 | Article publication date 01/03/2011

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ABSTRACT

INTRODUCTION 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. DEVELOPMENT. 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. CONCLUSION. 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. KeywordsADHD Dihydrotetrabenazyne (TBZOH)Methylphenidate Vesicular monoamine transporter VMAT2 CategoriesNeuropediatría Neuropsiquiatría

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Involvement of vesicular monoamine transporter in attention deficit hyperactivity disorder

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