Basal forebrain chemogenetic inhibition disrupts the superior complex movement control of goal-tracking rats.

Sign- and goal-tracking behavior signifies the influence of opposed cognitive-motivational styles, with the former being characterized by a tendency for approaching and contacting reward cues, including a readiness for attending, bottom-up, to salient cues, and a relatively greater vulnerability for developing and maintaining addiction-like behaviors. We previously demonstrated that these styles also impact the cognitive-motor interactions that are taxed during traversal of dynamic surfaces, with goal-trackers (GTs) making less movement errors and falling less frequently than sign-trackers (STs). The present experiment tested the hypothesis that complex movement control in GTs, but not STs, depends on activation of the basal forebrain projection system to telencephalic regions. Chemogenetic inhibition of the basal forebrain increased movement errors and falls in GTs during traversal of a rotating zigzag rod but had no significant effect on the relatively lower performance of STs. Neurochemical evidence confirmed the efficacy of the inhibitory designer receptor exclusively activated by designer drug (DREADD). Administration of clozapine-N-oxide (CNO) had no significant effect in GTs not expressing the DREADD. These results indicate that GTs, but not STs, activate the basal forebrain projection system to mediate their relatively superior ability for complex movement control. STs may also serve as an animal model in research on the role of basal forebrain systems in aging- and Parkinson's disease-associated falls. (PsycINFO Database Record (c) 2019 APA, all rights reserved).