title: The effects of manipulations of attentional demand on cortical acetylcholine release.
abstract: In vivo microdialysis was used to measure acetylcholine (ACh) efflux in the frontoparietal cortex while rats performed in one of two operant tasks. One task was designed and validated to generate measures of sustained attention, while the other task was designed to minimize explicit demands on sustained attentional resources (low-demand task). Transferring animals from the baseline environment into the operant chambers robustly increased cortical ACh efflux regardless of subsequent task demands. Performance in the sustained attention task further increased frontoparietal ACh efflux, and these increases were not observed when animals were simply exposed to the operant chamber without task performance. Manipulations of the task parameters within a session, to either increase or decrease explicit demands on sustained attention, were not associated with fluctuations in ACh efflux. Unexpectedly, performance in the low-demand task was also associated with significant increases in ACh efflux that were similar to those observed during the sustained attention task. However, widespread depletions of cortical cholinergic inputs produced by intra-basalis infusions of 192 IgG-saporin failed to impair performance in the low-demand task, suggesting that cholinergic transmission is not necessary for performance in this task. The present results indicate that although a wider range of instrumental processes than previously hypothesized are associated with increases in cortical ACh release, the dependence of performance on the integrity of cortical cholinergic inputs may be limited to tasks with explicit attentional demands.
authors.affiliation: Department of Psychology, The Ohio State University, Columbus, OH 43210, USA.
authors.forename: A M
authors.initials: AM
authors.lastname: Himmelheber
authors.forename: M
authors.initials: M
authors.lastname: Sarter
authors.forename: J P
authors.initials: JP
authors.lastname: Bruno
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D000911:Antibodies, Monoclonal; D001288:Attention / Q000502:physiology*; D002540:Cerebral Cortex / Q000378:metabolism* / Q000502:physiology*; D018678:Cholinergic Agents; D003216:Conditioning, Operant / Q000502:physiology; D005108:Extinction, Psychological / Q000502:physiology; D007839:Functional Laterality / Q000502:physiology; D006651:Histocytochemistry; D000922:Immunotoxins; D008297:Male; D017551:Microdialysis; D009699:N-Glycosyl Hydrolases; D010275:Parasympathetic Nervous System / Q000502:physiology; D010296:Parietal Lobe / Q000378:metabolism / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology; D051381:Rats; D011914:Rats, Inbred BN; D017207:Rats, Sprague-Dawley; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins
chemical_list: C085696:192 IgG-saporin; D000911:Antibodies, Monoclonal; D018678:Cholinergic Agents; D000922:Immunotoxins; D054789:Ribosome Inactivating Proteins, Type 1; D009699:N-Glycosyl Hydrolases; D000076985:Saporins; D000109:Acetylcholine