Induction of heat shock proteins and motor function deficits after focal cerebellar injury.
A weight drop model of focal cerebellar injury was used to identify heat shock protein induction and motor function deficits in the anesthetized, adult male, Sprague-Dawley rat. All animals were trained on a beam walking test prior to surgery. Groups of animals received severe, mild or sham weight drop injury to the lateral/paravermal region of the cerebellum. The mild and sham-injured animals showed no motor deficits in the beam walking test, whereas animals with severe cerebellar injury showed significant motor deficits in the beam walking test that approached recovery of motor function 20 days after injury. Following severe injury, induction of heat shock protein of 27kDa was observed in Purkinje cells and in neurons of the deep cerebellar nuclei, as well as Bergmann glial cells, glial cells located in the granule cell layer and the underlying white matter. Following mild injury, heat shock protein of 27kDa induction was observed in Purkinje cells and glial cells, but not in neurons of the deep cerebellar nuclei. The labeled Purkinje cells were widely distributed in the ipsilateral cerebellar cortex. Many of the glial cells that were immunostained with heat shock protein of 27kDa co-localized with cells immunoreactive for glial fibrillary acidic protein. After severe injury, heat shock protein of 72kDa was localized mainly in granule cells at the site of the trauma and in the ipsilateral deep cerebellar nuclei whereas, after mild injury, light labeling was observed only in the granule cell layer. The results demonstrate that focal cerebellar injury has profound effects on motor behavior and induces different families of heat shock proteins in specific groups of neurons and glial cells in the cerebellum.
Allen
G V
GV
Department of Anatomy & Neurobiology, Faculty of Medicine, Dalhousie University, Nova Scotia, B3H 4H7, Halifax, Canada. gva@is.dal.ca
Chase
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D000768:Anesthesia, General; D000818:Animals; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology*; D002529:Cerebellar Nuclei / Q000473:pathology / Q000503:physiopathology; D002531:Cerebellum / Q000473:pathology / Q000502:physiology / Q000503:physiopathology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D055551:HSP27 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000032:analysis / Q000096:biosynthesis*; D007150:Immunohistochemistry; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009363:Neoplasm Proteins / Q000032:analysis / Q000096:biosynthesis*; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011689:Purkinje Cells / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values
D005904:Glial Fibrillary Acidic Protein; D055551:HSP27 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C486114:Hspb1 protein, rat; D009363:Neoplasm Proteins