title: Deficits in attentional control: cholinergic mechanisms and circuitry-based treatment approaches.
abstract: The cognitive control of attention involves maintaining task rules in working memory (or "online"), monitoring reward and error rates, filtering distractors, and suppressing prepotent, and competitive responses. Weak attentional control increases distractibility and causes attentional lapses, impulsivity, and attentional fatigue. Levels of tonic cholinergic activity (changes over tens of seconds or minutes) modulate cortical circuitry as a function of the demands on cognitive control. Increased cholinergic modulation enhances the representation of cues, by augmenting cue-evoked activity in thalamic glutamatergic afferents, thereby increasing the rate of detection. Such cholinergic modulation is mediated primarily via α4β2* nicotinic acetylcholine receptors. Animal experiments and clinical trials in adult patients with ADHD indicate that attentional symptoms and disorders may benefit from drugs that stimulate this receptor. Tonic cholinergic modulation of cue-evoked glutamatergic transients in prefrontal regions is an essential component of the brain's executive circuitry. This circuitry model guides the development of treatments of deficits in attentional control.
authors: Department of Psychology, University of Michigan, Ann Arbor, MI 48103-8862, USA. msarter@umich.edu
authors: Martin
authors: M
authors: Sarter
authors: Giovanna
authors: G
authors: Paolone
mesh_terms: D000818:Animals; D001288:Attention / Q000502:physiology*; D001289:Attention Deficit Disorder with Hyperactivity / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology; D002799:Cholinergic Fibers / Q000187:drug effects / Q000502:physiology*; D003071:Cognition / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007175:Impulsive Behavior / Q000188:drug therapy / Q000503:physiopathology / Q000523:psychology; D009415:Nerve Net / Q000187:drug effects / Q000502:physiology*; D018722:Nicotinic Agonists / Q000494:pharmacology / Q000627:therapeutic use*; D011978:Receptors, Nicotinic / Q000502:physiology; D016896:Treatment Outcome
chemical_list: D018722:Nicotinic Agonists; D011978:Receptors, Nicotinic