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.

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.