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Neurochem Int. 2015 Mar;82:52-68. doi: 10.1016/j.neuint.2015.02.001. Epub 2015 Feb 12.

Does serotonin deficit mediate susceptibility to ADHD?

Author information

1
Department of Genetics, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India.
2
Department of Genetics, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India. Electronic address: knandago2007@gmail.com.

Abstract

The onset of attention-deficit-hyperactivity-disorder (ADHD) in childhood is characterized by developmentally inappropriate levels of hyperactivity, impulsivity and inattention. A chronic deficit of serotonin (5-HT) at the synapse may trigger symptoms of ADHD. This review focuses on neuro-anatomical, experimental and clinical pharmacological evidence, as well as the genetic underpinnings of serotoninergic involvement in the etiology of ADHD. Neuro-anatomical investigations suggest that serotonin through the orbitofrontal-striatal circuitry may regulate behavioral domains of hyperactivity and impulsivity in ADHD. Studies from animal models of ADHD indicate intimate interplay between 5-HT and dopaminergic neurotransmission. Selective serotonin re-uptake inhibitors, as also non-stimulant drugs acting on the 5-HT system are, however, clinically effective. They impart less severe side effects in patients with no risk of addiction. Oral administration of l-tryptophan, the amino acid precursor of 5-HT, significantly alleviates ADHD symptoms. Given the multifactorial nature of ADHD, candidate gene and genome-wide association studies have suggested that serotoninergic gene variants are associated with increased risk of ADHD with each locus individually exerting a modest effect on overall risk.

KEYWORDS:

ADHD; Animal model; Clinical pharmacology; Genetics; Neuroanatomy; Serotonin

PMID:
25684070
DOI:
10.1016/j.neuint.2015.02.001
[Indexed for MEDLINE]

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