title: Behavioral recovery and anatomical plasticity in adult rats after cortical lesion and treatment with monoclonal antibody IN-1.
abstract: We have previously reported that monoclonal antibody (mAb) IN-1 treatment after ischemic infarct in adult rats results in significant recovery of skilled forelimb use. Such recovery was correlated with axonal outgrowth from the intact, opposite motor cortex into deafferented subcortical motor areas. In the present study, we investigated the effects of mAb IN-1 treatment after adult sensorimotor cortex (SMC) aspiration lesion on behavioral recovery and neuroanatomical plasticity in the corticospinal tract. Adult rats underwent unilateral SMC aspiration lesion and treatment with either mAb IN-1 or a control Ab, or no treatment. Animals were then tested over a 6-week period in the skilled forelimb use task and the skilled ladder rung walking task. We found that animals treated with mAb IN-1 after SMC lesion fully recovered the use of forelimb reaching, but showed no improvement in digit grasping as tested in the skilled forelimb use task. The mAb IN-1 treatment group was also significantly improved as compared to control groups in the skilled ladder rung walking test. Furthermore, neuroanatomical tracing revealed a significant increase in the corticospinal projections into the deafferented motor areas of the spinal cord after mAb IN-1 treatment. These results indicate that treatment with mAb IN-1 after cortical aspiration lesion induces remodeling of motor pathways resulting in recovery in only certain behavioral tasks, suggesting that the cause of brain damage influences behavioral recovery after mAb IN-1 treatment.
authors.affiliation: Research and Neurology Service, Edward Hines Veterans Affairs Hospital, Hines, IL 60141, USA. aemeric@lumc.edu
authors.forename: April J
authors.initials: AJ
authors.lastname: Emerick
authors.forename: Gwendolyn L
authors.initials: GL
authors.lastname: Kartje
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D001710:Biotin / Q000031:analogs & derivatives* / Q000378:metabolism; D001927:Brain Diseases / Q000473:pathology / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000187:drug effects* / Q000293:injuries / Q000503:physiopathology; D002541:Cerebral Decortication / Q000379:methods; D003911:Dextrans / Q000378:metabolism; D007839:Functional Laterality; D006825:Hybridomas / Q000378:metabolism; D008297:Male; D009048:Motor Skills / Q000187:drug effects; D009185:Myelin Proteins / Q000276:immunology*; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D000070798:Nogo Proteins; D051381:Rats; D020318:Rats, Long-Evans; D020127:Recovery of Function / Q000187:drug effects*; D013997:Time Factors; D016138:Walking / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D003911:Dextrans; D009185:Myelin Proteins; D000070798:Nogo Proteins; C000603197:Rtn4 protein, rat; C076397:biotinylated dextran amine; D001710:Biotin