Spinal pathways involved in the control of forelimb motor function in rats.
There is increasing interest in developing rodent models for cervical spinal cord injury (SCI) and techniques to assess forelimb motor function. Previously, we demonstrated that in rats, complete unilateral hemisection at cervical level five (C5) permanently eliminated the ability to grip and caused severe impairments in food retrieval by the forepaw ipsilateral to the lesion [Anderson, K.D., Gunawan, A., Steward, O., 2005. Quantitative behavioral analysis of forepaw function after cervical spinal cord injury in rats: Relationship to the corticospinal tract. Exp. Neurol. 194, 161-174]. Here, we analyzed the functional consequences of partial lesions that damaged tracts/cells located in the medial vs. lateral portion of the spinal cord. Female Sprague-Dawley rats were trained on the Grip Strength Meter (GSM) and the food pellet reaching task. Rats then received either a "medial lesion" that destroyed an approximately 0.5 mm wide zone from the midline laterally (which included the dorsal column) or "lateral lesion" that destroyed the lateral column at C5 and were tested for 8 weeks. Rats with histologically-verified medial lesions exhibited a complete loss of gripping ability for 7 weeks post-injury; only 1 of 4 animals exhibited any recovery of grip strength, and this occurred at 54 days. In contrast, rats with lateral lesions exhibited deficits, but the majority (7/10) recovered the ability to grip by 43 days post-injury. Interestingly, when tested on the food retrieval task, rats with medial lesions exhibited deficits that recovered; rats with lateral lesions exhibited more permanent deficits. These results suggest that different spinal circuits are involved in recovery of grip strength vs. recovery of skilled reaching.
Anderson
Kim D
KD
Reeve-Irvine Research Center, University of California at Irvine College of Medicine, Department of Anatomy, Irvine, CA 92697-4292, USA.
Gunawan
Ardi
A
Steward
Oswald
O
D000222:Adaptation, Physiological / Q000502:physiology; D000818:Animals; D001710:Biotin / Q000031:analogs & derivatives; D003911:Dextrans; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000503:physiopathology*; D005260:Female; D005552:Forelimb / Q000294:innervation / Q000503:physiopathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D018737:Hand Strength / Q000502:physiology; D009048:Motor Skills / Q000502:physiology; D009068:Movement / Q000502:physiology; D009069:Movement Disorders / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D053580:Muscle Strength / Q000502:physiology; D053581:Muscle Strength Dynamometer; D018908:Muscle Weakness / Q000209:etiology / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology; D011712:Pyramidal Tracts / Q000502:physiology / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*; D014855:Wallerian Degeneration / Q000473:pathology / Q000503:physiopathology
D003911:Dextrans; D005904:Glial Fibrillary Acidic Protein; C076397:biotinylated dextran amine; D001710:Biotin