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J Neurosci Methods. 2007 Apr 15;161(2):185-98. Epub 2006 Dec 21.

Neurobiology of animal models of attention-deficit hyperactivity disorder.

Author information

1
Department of Human Biology, University of Cape Town, Anzio Road, Observatory 7925, South Africa. Vivienne.Russell@curie.uct.ac.za

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.

PMID:
17275916
DOI:
10.1016/j.jneumeth.2006.12.005
[Indexed for MEDLINE]
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