Literature DB >> 2358536

Distribution of calcium-activated protease calpain in the rat brain.

L S Perlmutter1, C Gall, M Baudry, G Lynch.   

Abstract

Calpain is a calcium-activated neutral protease that degrades a number of cytoskeletal proteins. It may participate in the maintenance of the cytoskeleton and in the rapid turnover of structural proteins associated with synaptic plasticity. Calpain may also be involved in the neurodegeneration that accompanies aging and age-related diseases. To aid in the interpretation of disease-related alterations in staining patterns, the present study examined calpain's normal distribution in the mammalian brain and spinal cord. A monoclonal antibody was employed with the avidin-biotin-peroxidase immunocytochemical technique on samples of rat tissue. Glia (astrocytes, microglia) and virtually all neurons were immunopositive, although neuronal processes exhibited varying staining patterns. The axonal staining pattern depended upon either the origin or destination of the process: those axons remaining within the brain (e.g., corpus callosum) were only lightly immunoreactive, whereas spinal cord and peripheral axons (trigeminal nerve) were more darkly labeled. The architecture of the dendritic tree determined the dendritic staining pattern: neurons with prominent apical and basal dendritic trees (e.g., pyramidal cells) were immunolabeled along their entire extent; labeling of multipolar cells (e.g., hilar cells of dentate gyrus) was limited to the proximal dendrites. The ubiquitous distribution of calpain argues against a primary role for the enzyme in the regional pattern of neuronal death seen in Alzheimer's disease. An alteration in the concentration, localization, or inhibition of the enzyme could, however, lead to the abnormal accumulations of cytoskeletal elements seen with the disease.

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Year:  1990        PMID: 2358536     DOI: 10.1002/cne.902960207

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


  14 in total

1.  The effects of the dynamic state of the cytoskeleton on neuronal plasticity.

Authors:  T A Zapara; O G Simonova; A A Zharkikh; A S Ratushnyak
Journal:  Neurosci Behav Physiol       Date:  2000 May-Jun

Review 2.  The Role of Proteases in Hippocampal Synaptic Plasticity: Putting Together Small Pieces of a Complex Puzzle.

Authors:  Ivan L Salazar; Margarida V Caldeira; Michele Curcio; Carlos B Duarte
Journal:  Neurochem Res       Date:  2015-11-07       Impact factor: 3.996

Review 3.  Calpain and synaptic function.

Authors:  Hai-Yan Wu; David R Lynch
Journal:  Mol Neurobiol       Date:  2006-06       Impact factor: 5.590

Review 4.  Review of the multiple aspects of neurofilament functions, and their possible contribution to neurodegeneration.

Authors:  Rodolphe Perrot; Raphael Berges; Arnaud Bocquet; Joel Eyer
Journal:  Mol Neurobiol       Date:  2008-07-23       Impact factor: 5.590

5.  NMDA receptor activation and calpain contribute to disruption of dendritic spines by the stress neuropeptide CRH.

Authors:  Adrienne L Andres; Limor Regev; Lucas Phi; Ronald R Seese; Yuncai Chen; Christine M Gall; Tallie Z Baram
Journal:  J Neurosci       Date:  2013-10-23       Impact factor: 6.167

6.  Immunohistochemical distribution and electron microscopic subcellular localization of the proteasome in the rat CNS.

Authors:  E Mengual; P Arizti; J Rodrigo; J M Giménez-Amaya; J G Castaño
Journal:  J Neurosci       Date:  1996-10-15       Impact factor: 6.167

7.  Maitotoxin induces calpain but not caspase-3 activation and necrotic cell death in primary septo-hippocampal cultures.

Authors:  X Zhao; B R Pike; J K Newcomb; K K Wang; R M Posmantur; R L Hayes
Journal:  Neurochem Res       Date:  1999-03       Impact factor: 3.996

Review 8.  The pathogenic activation of calpain: a marker and mediator of cellular toxicity and disease states.

Authors:  P W Vanderklish; B A Bahr
Journal:  Int J Exp Pathol       Date:  2000-10       Impact factor: 1.925

Review 9.  Role of calpains in the injury-induced dysfunction and degeneration of the mammalian axon.

Authors:  Marek Ma
Journal:  Neurobiol Dis       Date:  2013-08-19       Impact factor: 5.996

10.  Compromised mitochondrial function results in dephosphorylation of tau through a calcium-dependent process in rat brain cerebral cortical slices.

Authors:  S G Norman; G V Johnson
Journal:  Neurochem Res       Date:  1994-09       Impact factor: 3.996

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