title: Behavioral training increases local astrocytic metabolic activity but does not alter outcome of mild transient ischemia.
abstract: Functional neurological outcome after transient ischemia might be improved by timely therapeutic intervention. To determine if restorative behavioral therapy influences damage, improves task learning, or alters astrocyte metabolic activity after ischemia, rats (food-restricted to 85% of free-feeding weight) were (a) first trained to respond on one of two levers under a fixed-ratio 20 schedule of food presentation (FR20), then (b) subjected to sham manipulation of carotid arteries or 10 min ischemia by four-vessel occlusion, followed by (c) 4 days of operant testing or inactivity, (d) then all rats were tested under a FR20 lever reversal task for 4 weeks, and (e) 3 days after the last behavioral session astrocyte metabolism was assayed by local uptake of [2-14C]acetate. Mild loss of hippocampal neurons occurred in ischemic rats with or without training after ischemia. Glial fibrillary acidic protein-positive astrocytes were present in similar numbers throughout brains of sham control and ischemic rats. Mild ischemia did not impair learning, and no changes in FR20 reversal learning were detected in sham vs. ischemic rats. Net [14C]acetate uptake was unaffected by ischemia but [14C]acetate uptake increased 15-24% (P<0.05; n=12-15/group) in specific structures (caudate, primary motor and sensorimotor cortex, CA1 hippocampus, subcortical white matter) in the pooled groups of rats that had 4 days FR20 testing vs. inactivity before reversal learning. 'Behavioral therapy' (operant testing on the 4 days immediately following either sham manipulation or ischemia) did not alter ischemic outcome, but was associated with higher acetate utilization in regions involved in motor activities.
authors.affiliation: Department of Neurology, University of Arkansas for Medical Sciences, 4301 W. Markham St., Little Rock 72205, USA. dinelgeralda@uams.edu
authors.forename: Gerald A
authors.initials: GA
authors.lastname: Dienel
authors.forename: Nancy F
authors.initials: NF
authors.lastname: Cruz
authors.forename: Kelly
authors.initials: K
authors.lastname: Ball
authors.forename: David
authors.initials: D
authors.lastname: Popp
authors.forename: Murat
authors.initials: M
authors.lastname: Gokden
authors.forename: Scott
authors.initials: S
authors.lastname: Baron
authors.forename: Dean
authors.initials: D
authors.lastname: Wright
authors.forename: Galen R
authors.initials: GR
authors.lastname: Wenger
mesh_terms: D019342:Acetic Acid / Q000378:metabolism*; D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D002250:Carbon Radioisotopes; D003072:Cognition Disorders / Q000209:etiology / Q000628:therapy; D003216:Conditioning, Operant; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000150:complications / Q000378:metabolism / Q000534:rehabilitation*; D007858:Learning; D008297:Male; D009043:Motor Activity; D009474:Neurons / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002250:Carbon Radioisotopes; D005904:Glial Fibrillary Acidic Protein; D019342:Acetic Acid