Dopamine vs noradrenaline: inverted-U effects and ADHD theories.

Abstract

The aim of the present study was to review the dopamine theory of attention-deficit-hyperactivity disorder (ADHD), in light of recent use of noradrenergic therapies. A historical review of pharmacological theories of ADHD was conducted, including inverted-U, spatial working memory and neural circuit aspects. Pharmacological advances, including animal and human studies of dopaminergic and noradrenergic mechanisms at the prefrontal cortex (PFC), indicate that alpha-2A adrenoreceptor stimulation results in increased dendritic firing during delay periods for preferred directions, while moderate levels of D1 receptor stimulation result in reduction of delay-related firing to non-preferred directions, allowing representational control in the PFC. Recent studies of the COMT val/met gene and stimulant medication response may help explain variation in inverted-U responses in individuals. Further studies utilizing delay-related firing paradigms should be useful in the investigation of attentional syndromes, and responses to newer pharmacological treatments.

• Authors: Florence Levy
• Journal: The Australian and New Zealand journal of psychiatry (Aust N Z J Psychiatry) Vol. 43 Issue 2 Pg. 101-8 (Feb 2009) ISSN: 1440-1614 [Electronic] England
• PMID: 19153917 (Publication Type: Journal Article, Review)

Chemical References

• Adrenergic Uptake Inhibitors
• Adrenergic alpha-Agonists
• DRD4 protein, human
• Propylamines
• Receptors, Adrenergic, alpha-2
• Receptors, Dopamine D4
• Guanfacine
• Atomoxetine Hydrochloride
• Catechol O-Methyltransferase
• Dopamine
• Norepinephrine

Topics

• Adrenergic Uptake Inhibitors (pharmacology, therapeutic use)
• Adrenergic alpha-Agonists (pharmacology, therapeutic use)
• Alleles
• Animals
• Atomoxetine Hydrochloride
• Attention Deficit Disorder with Hyperactivity (drug therapy, genetics, metabolism)
• Catechol O-Methyltransferase (genetics)
• Dopamine (metabolism)
• Guanfacine (pharmacology, therapeutic use)
• Humans
• Memory, Short-Term (drug effects)
• Nerve Net (drug effects, metabolism)
• Norepinephrine (metabolism)
• Polymorphism, Genetic (genetics)
• Prefrontal Cortex (drug effects, metabolism)
• Propylamines (pharmacology, therapeutic use)
• Receptors, Adrenergic, alpha-2 (drug effects, metabolism)
• Receptors, Dopamine D4 (genetics)
• Space Perception (drug effects)
• Thalamus (metabolism)