(cont)
It has been proposed that the alteration of behavioral adaptation in ß2−/− mice, coupled with unimpaired memory and anxiety, may model cognitive impairment observed in human disorders [4] such as attention-deficit hyperactivity disorder (ADHD) [32], or even in autism [5]. This proposition relies upon the idea that behavioral flexibility is controlled by an adequate hierarchization of motivations, a process known to mobilize prefrontal and cingulate cortex. ADHD symptoms such as inattention lack of inhibitory control, and hyperactivity and prefrontal involvement indeed resemble ß2−/− behavioral deficits, and fit well with nAChR localization and function. Yet, the possible contribution of prefrontal cortex and higher-level top-down processes in open-field behaviors is at this stage not clear.