title: Neurotoxic lesions of the caudate-putamen on a reaching for food task in the rat: acute sensorimotor neglect and chronic qualitative motor impairment follow lateral lesions and improved success follows medial lesions.
abstract: Reaching for food, or skilled reaching, is used as a test of basal ganglia function in preclinical studies as well as studies of human neurological conditions. Although changes in the end-point measure of success document the effects of neurotoxic cellular damage to the caudate-putamen and its treatment in rodents, there has been no examination of the cause of change in success after neurotoxic lesions of the striatum. This objective was addressed in the present study, in which rats trained to reach for single food pellets with one forelimb, received contralateral quinolinic acid or ibotenic acid lesions of the medial and lateral caudate-putamen. Over 21 postsurgical days, reaching performance was scored for success and qualitative changes in movement elements were examined using frame-by-frame video analysis. In the acute postoperative period, extending over 3 to 4 days, the rats with lateral lesions transported their forelimb and grasped the food, but then ignored the food and did not withdraw their limb to their mouth. After recovery of the withdrawal movement, the rats displayed chronic qualitative impairments in the rotatory movements of aiming, pronating, and supinating the forepaw. Medial quinolinic lesions improved success relative to control rats and did not change qualitative aspects of limb movement. The acute dissociation between transport and withdrawal, the chronic qualitative changes in movement elements, and the differential effect of medial and lateral injury on success, support a complex contribution of the caudate-putamen to skilled reaching that includes sensorimotor neglect, and quantitative and qualitative motoric changes.
authors.affiliation: Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta, Canada T1K 3M4. Whishaw@uleth.ca
authors.forename: I Q
authors.initials: IQ
authors.lastname: Whishaw
authors.forename: F
authors.initials: F
authors.lastname: Zeeb
authors.forename: C
authors.initials: C
authors.lastname: Erickson
authors.forename: R J
authors.initials: RJ
authors.lastname: McDonald
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D001930:Brain Injuries / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D016923:Cell Death / Q000187:drug effects; D003216:Conditioning, Operant / Q000187:drug effects / Q000502:physiology; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology; D007839:Functional Laterality / Q000187:drug effects; D007051:Ibotenic Acid / Q000633:toxicity; D008297:Male; D009068:Movement / Q000187:drug effects; D017072:Neostriatum / Q000293:injuries* / Q000503:physiopathology; D009498:Neurotoxins / Q000633:toxicity; D011597:Psychomotor Performance / Q000187:drug effects / Q000502:physiology*; D017378:Quinolinic Acid / Q000633:toxicity; D051381:Rats; D020318:Rats, Long-Evans; D020127:Recovery of Function; D013997:Time Factors
chemical_list: D009498:Neurotoxins; D007051:Ibotenic Acid; D017378:Quinolinic Acid