Reprint of "Neurobiology of animal models of attention-deficit hyperactivity disorder".

摘要: Attention-deficit hyperactivity disorder (ADHD) is a heterogeneous, highly heritable, resulting from complex gene-gene and gene-environment interactions. The defining symptoms of hyperactivity, impulsivity impaired sustained attention are not unique to ADHD. It therefore surprising that animals with distinctly different neural defects model the behavioural characteristics disorder. Consistent ADHD being developmental disorder, animal models either genetic (spontaneously hypertensive rats (SHR), dopamine transporter (DAT) knock-out mice, SNAP-25 mutant mice expressing thyroid receptor) or have suffered an insult central nervous system during early stages development (anoxia, 6-hydroxydopamine). appears transmission by direct disruption dopaminergic more general impairment neurotransmission gives rise compensatory changes in monoaminergic systems sufficient completely normalize function. In general, results obtained studies suggest neurons functionally impaired. However, evidence some suggests noradrenergic serotonergic neurotransmitter may be target drugs ameliorate symptoms.