期刊
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
卷 99, 期 2, 页码 211-216出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbb.2011.01.020
关键词
Guanfacine; Prefrontal cortex; Attention deficit/hyperactivity disorder; Catecholamines; Norepinephrine; Alpha-2A adrenergic receptors
资金
- PHS [PO1 AG030004]
- Shire Development, Wayne, PA
- Shire Pharmaceuticals
- Ortho-McNeil-Janssen and Shire
- [AG06036]
- [1RL1AA017536]
- [U54RR024350]
The primary symptoms of attention deficit/hyperactivity disorder (ADHD) include poor impulse control and impaired regulation of attention. Research has shown that the prefrontal cortex (PFC) is essential for the top-down regulation of attention, behavior, and emotion, and that this brain region is underactive in many patients with ADHD. The PFC is known to be especially sensitive to its neurochemical environment; relatively small changes in the levels of norepinephrine and dopamine can produce significant changes in its function. Therefore, alterations in the pathways mediating catecholamine transmission can impair PFC function, while medications that optimize catecholamine actions can improve PFC regulation of attention, behavior, and emotion. This article reviews studies in animals showing that norepinephrine and dopamine enhance PFC function through actions at postsynaptic alpha(2A)-adrenoceptors and dopamine D1-receptors, respectively. Stimulant medications and atomoxetine appear to enhance PFC function through increasing endogenous adrenergic and dopaminergic stimulation of alpha(2A)-receptors and D1-receptors. In contrast, guanfacine mimics the enhancing effects of norepinephrine at postsynaptic alpha(2A)-receptors in the PFC, strengthening network connectivity. Stronger PFC regulation of attention, behavior, and emotion likely contributes to the therapeutic effects of these medications for the treatment of ADHD. (C) 2011 Elsevier Inc. All rights reserved.
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