Animal models of attention-deficit hyperactivity disorder

<p>Abstract</p> <p>Although animals cannot be used to study complex human behaviour such as language, they do have similar basic functions. In fact, human disorders that have animal models are better understood than disorders that do not. ADHD is a heterogeneous disorder. The relat...

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Main Authors: Sagvolden Terje, Russell Vivienne A, Johansen Espen
Format: Article
Language:English
Published: BMC 2005-07-01
Series:Behavioral and Brain Functions
Online Access:http://www.behavioralandbrainfunctions.com/content/1/1/9
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spelling doaj-8c59ab7157b3403f882dee1f072100c92020-11-25T02:49:13ZengBMCBehavioral and Brain Functions1744-90812005-07-0111910.1186/1744-9081-1-9Animal models of attention-deficit hyperactivity disorderSagvolden TerjeRussell Vivienne AJohansen Espen<p>Abstract</p> <p>Although animals cannot be used to study complex human behaviour such as language, they do have similar basic functions. In fact, human disorders that have animal models are better understood than disorders that do not. ADHD is a heterogeneous disorder. The relatively simple nervous systems of rodent models have enabled identification of neurobiological changes that underlie certain aspects of ADHD behaviour. Several animal models of ADHD suggest that the dopaminergic system is functionally impaired. Some animal models have decreased extracellular dopamine concentrations and upregulated postsynaptic dopamine D1 receptors (DRD1) while others have increased extracellular dopamine concentrations. In the latter case, dopamine pathways are suggested to be hyperactive. However, stimulus-evoked release of dopamine is often decreased in these models, which is consistent with impaired dopamine transmission. It is possible that the behavioural characteristics of ADHD result from impaired dopamine modulation of neurotransmission in cortico-striato-thalamo-cortical circuits. There is considerable evidence to suggest that the noradrenergic system is poorly controlled by hypofunctional α<sub>2</sub>-autoreceptors in some models, giving rise to inappropriately increased release of norepinephrine. Aspects of ADHD behaviour may result from an imbalance between increased noradrenergic and decreased dopaminergic regulation of neural circuits that involve the prefrontal cortex. Animal models of ADHD also suggest that neural circuits may be altered in the brains of children with ADHD. It is therefore of particular importance to study animal models of the disorder and not normal animals. Evidence obtained from animal models suggests that psychostimulants may not be acting on the dopamine transporter to produce the expected increase in extracellular dopamine concentration in ADHD. There is evidence to suggest that psychostimulants may decrease motor activity by increasing serotonin levels. In addition to providing unique insights into the neurobiology of ADHD, animal models are also being used to test new drugs that can be used to alleviate the symptoms of ADHD.</p> http://www.behavioralandbrainfunctions.com/content/1/1/9
collection DOAJ
language English
format Article
sources DOAJ
author Sagvolden Terje
Russell Vivienne A
Johansen Espen
spellingShingle Sagvolden Terje
Russell Vivienne A
Johansen Espen
Animal models of attention-deficit hyperactivity disorder
Behavioral and Brain Functions
author_facet Sagvolden Terje
Russell Vivienne A
Johansen Espen
author_sort Sagvolden Terje
title Animal models of attention-deficit hyperactivity disorder
title_short Animal models of attention-deficit hyperactivity disorder
title_full Animal models of attention-deficit hyperactivity disorder
title_fullStr Animal models of attention-deficit hyperactivity disorder
title_full_unstemmed Animal models of attention-deficit hyperactivity disorder
title_sort animal models of attention-deficit hyperactivity disorder
publisher BMC
series Behavioral and Brain Functions
issn 1744-9081
publishDate 2005-07-01
description <p>Abstract</p> <p>Although animals cannot be used to study complex human behaviour such as language, they do have similar basic functions. In fact, human disorders that have animal models are better understood than disorders that do not. ADHD is a heterogeneous disorder. The relatively simple nervous systems of rodent models have enabled identification of neurobiological changes that underlie certain aspects of ADHD behaviour. Several animal models of ADHD suggest that the dopaminergic system is functionally impaired. Some animal models have decreased extracellular dopamine concentrations and upregulated postsynaptic dopamine D1 receptors (DRD1) while others have increased extracellular dopamine concentrations. In the latter case, dopamine pathways are suggested to be hyperactive. However, stimulus-evoked release of dopamine is often decreased in these models, which is consistent with impaired dopamine transmission. It is possible that the behavioural characteristics of ADHD result from impaired dopamine modulation of neurotransmission in cortico-striato-thalamo-cortical circuits. There is considerable evidence to suggest that the noradrenergic system is poorly controlled by hypofunctional α<sub>2</sub>-autoreceptors in some models, giving rise to inappropriately increased release of norepinephrine. Aspects of ADHD behaviour may result from an imbalance between increased noradrenergic and decreased dopaminergic regulation of neural circuits that involve the prefrontal cortex. Animal models of ADHD also suggest that neural circuits may be altered in the brains of children with ADHD. It is therefore of particular importance to study animal models of the disorder and not normal animals. Evidence obtained from animal models suggests that psychostimulants may not be acting on the dopamine transporter to produce the expected increase in extracellular dopamine concentration in ADHD. There is evidence to suggest that psychostimulants may decrease motor activity by increasing serotonin levels. In addition to providing unique insights into the neurobiology of ADHD, animal models are also being used to test new drugs that can be used to alleviate the symptoms of ADHD.</p>
url http://www.behavioralandbrainfunctions.com/content/1/1/9
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