Dopamine hypofunction possibly results from a defect in glutamate-stimulated release of dopamine in the nucleus accumbens shell of a rat model for attention deficit hyperactivity disorder–the spontaneously hypertensive rat.
Abstract
RUSSELL, V.A. Dopamine hypofunction possibly results from a defect in glutamate-stimulated release of dopamine in the nucleus accumbens shell of a rat model for attention deficit hyperactivity disorder-the spontaneously hypertensive rat. NEUROSCI. BIOBEHAV. REV.27(2003). Disturbances in glutamate, dopamine and norepinephrine function in the brain of a genetic animal model for attention-deficit hyperactivity disorder (ADHD), the spontaneously hypertensive rat (SHR), and information obtained from patients with ADHD, suggest a defect in neuronal circuits that are required for reward-guided associative learning and memory formation. Evidence derived from (i). the neuropharmacology of drugs that are effective in treating ADHD symptoms, (ii). molecular genetic and neuroimaging studies of ADHD patients, as well as (iii). the behaviour and biochemistry of animal models, suggests dysfunction of dopamine neurons. SHR have decreased stimulation-evoked release of dopamine as well as disturbances in the regulation of norepinephrine release and impaired second messenger systems, cAMP and calcium. In addition, evidence supports a selective deficit in the nucleus accumbens shell of SHR which could contribute to impaired reinforcement of appropriate behaviour.
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SHR rats display reduced DA signaling and increased DAT expression, similar to ADHD patients.
“Further, SHR rats display reduced DA signaling and increased DA transporter (DAT) expression, similar to ADHD patients (Russell et al., 1995; Russell, 2003; Heal et al., 2008; Roessner et al., 2010).”
From The Effects of Methylphenidate on Goal-directed Behavior in a Rat Model of ADHD (2015) · cites this paper as Russell, 2003
Excessive DA stimulation might cause PFC dysfunction leading to impaired inhibition of undesirable behavior and a deficit in sustaining attention.
“However, excessive DA stimulation might cause PFC dysfunction leading to impaired inhibition of undesirable behavior, and a deficit in sustaining attention, as these two behaviors are highly regulated by dopaminergic release in the PFC (Russell, 2003; Brennan and Arnsten, 2008; Arnsten, 2011).”
From The Effects of Methylphenidate on Goal-directed Behavior in a Rat Model of ADHD (2015) · cites this paper as Russell, 2003
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- Authors
- Russell, V. A.
- Affiliations
- University of Cape Town (ZA)
- Corresponding author
- Russell, Vivienne Ann
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2003-11
- Volume
- 27
- Issue
- 7
- Pages
- 671-682
- ISSN
- 0149-7634 (ISSN-L)
- OpenAlex
- W2028729354
- Cited by
- 107
- References
- 10
- Citations by year
- 2025: 4 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 5 · 2015: 6 · 2014: 3 · 2013: 2 · 2012: 9
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- South African Medical Research Council
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- University of Cape Town
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- attention deficit hyperactivity disorder, spontaneously hypertensive rats, nucleus accumbens shell, noradrenaline release, cAMP signaling, calcium signaling, reinforcement, animal model of ADHD
- MeSH terms
- Animals, Attention Deficit Disorder with Hyperactivity, Disease Models, Animal, Dopamine, Humans, Nucleus Accumbens, Rats, Inbred SHR, Rats, Inbred Strains, Rats, Inbred WKY, Receptors, Dopamine, Mice, Knockout, Glutamic Acid, Mice, Rats
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