Research article summary (published 28 Nov 2007):

Reprint of "Neurobiology of animal models of attention-deficit hyperactivity disorder".

Full Abstract

Attention-deficit hyperactivity disorder (ADHD) is a heterogeneous, highly heritable, disorder resulting from complex gene-gene and gene-environment interactions. The defining symptoms of hyperactivity, impulsivity and impaired sustained attention are not unique to ADHD. It is therefore not surprising that animals with distinctly different neural defects model the behavioural characteristics of the disorder. Consistent with ADHD being a developmental disorder, animal models are either genetic (spontaneously hypertensive rats (SHR), dopamine transporter (DAT) knock-out mice, SNAP-25 mutant mice, mice expressing a mutant thyroid receptor) or have suffered an insult to the central nervous system during the early stages of development (anoxia, 6-hydroxydopamine). It appears that neural transmission is impaired by either direct disruption of dopaminergic transmission or a more general impairment of neurotransmission that gives rise to compensatory changes in monoaminergic systems that are not sufficient to completely normalize neural function. In general, results obtained with animal studies suggest that dopamine neurons are functionally impaired. However, evidence obtained from some animal models suggests that the noradrenergic and serotonergic neurotransmitter systems may be the target of drugs that ameliorate ADHD symptoms.

Author information

Author/s: Russell, Vivienne Ann (VA);

Affiliation: Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Anzio Road, Observatory 7925, South Africa. Vivienne.Russell(-atsign-)curie.uct.ac.za

Journal and publication information

Publication Type: Corrected and Republished Article; Duplicate Publication; Journal Article; Research Support, Non-U.S. Gov't; Review

Journal: Journal of neuroscience methods (J Neurosci Methods), published in Netherlands. (Language: eng)

Reference: 2007-Nov; vol 166 (issue 2) : pp I-XIV

Dates: Created 2007/11/05; Completed 2008/02/14;

PMID: 17980763, status: MEDLINE (last retrieved date: 2/18/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

Comments and Corrections

RepublishedFrom: J Neurosci Methods. 2007 Apr 15;161(2):185-98. (PMID: 17275916)

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Animals Attention Deficit Disorder with Hyperactivity - genetics; physiopathology Disease Models, Animal Dopamine Plasma Membrane Transport Proteins - deficiency Humans Mice

Mice, Transgenic Mutation Neurobiology Rats Rats, Inbred SHR Synaptosomal-Associated Protein 25 - genetics

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Dopamine Plasma Membrane Transport Proteins (0) ; Synaptosomal-Associated Protein 25 (0)

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