Cholinergic modulation of visual attention and working memory: dissociable effects of basal forebrain 192-IgG-saporin lesions and intraprefrontal infusions of scopolamine.
Two experiments examined the effects of reductions in cortical cholinergic function on performance of a novel task that allowed for the simultaneous assessment of attention to a visual stimulus and memory for that stimulus over a variable delay within the same test session. In the first experiment, infusions of the muscarinic receptor antagonist scopolamine into the medial prefrontal cortex (mPFC) produced many omissions but did not impair rats' ability to correctly detect a brief visual stimulus. However, these animals were highly impaired in remembering the location of that stimulus following a delay period, although in a delay-independent manner. In the second experiment, another group of animals with selective 192 IgG-saporin lesions of the nucleus basalis magnocellularis (nBM) were not impaired under conditions of low-attentional demand. However, when the stimulus duration was reduced, a significant memory impairment was observed, but similar to the results of the first experiment, the nBM-lesioned animals were not impaired in attentional accuracy, although aspects of attention were compromised (e.g., omissions). These findings demonstrate that (1) cortical cholinergic depletion produces dissociable deficits in attention and memory, depending on the task demands, (2) delay-independent mnemonic deficits produced by scopolamine are probably due to impairments other than simple inattention, and (3) working memory deficits are not simply dependent on attentional difficulties per se. Together, these findings implicate the nBM cortical cholinergic system in both attentional and mnemonic processing.
Chudasama
Yogita
Y
Cambridge University, Department of Experimental Psychology, Cambridge CB2 3EB, UK. Yogita@ln.nimh.nih.gov
Dalley
Jeffrey W
JW
Nathwani
Falguni
F
Bouger
Pascale
P
Robbins
Trevor W
TW
Nathwani
Falgyni
F
D000109:Acetylcholine / Q000502:physiology*; D000759:Adjuvants, Anesthesia / Q000494:pharmacology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001288:Attention / Q000187:drug effects / Q000502:physiology*; D020532:Basal Nucleus of Meynert / Q000502:physiology; D018678:Cholinergic Agents / Q000494:pharmacology; D000922:Immunotoxins / Q000494:pharmacology; D008297:Male; D008568:Memory / Q000502:physiology; D008570:Memory, Short-Term / Q000187:drug effects / Q000502:physiology*; D009699:N-Glycosyl Hydrolases; D017397:Prefrontal Cortex / Q000187:drug effects / Q000502:physiology*; D016548:Prosencephalon / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins; D012601:Scopolamine / Q000494:pharmacology; D014796:Visual Perception / Q000187:drug effects / Q000502:physiology*
C085696:192 IgG-saporin; D000759:Adjuvants, Anesthesia; D000911:Antibodies, Monoclonal; D018678:Cholinergic Agents; D000922:Immunotoxins; D054789:Ribosome Inactivating Proteins, Type 1; D012601:Scopolamine; D009699:N-Glycosyl Hydrolases; D000076985:Saporins; D000109:Acetylcholine