An immunocytochemical study of calpain II in the hippocampus of rats injected with kainate

被引:7
作者
Ong, WY
Garey, LJ
Tan, KK
机构
[1] CHARING CROSS & WESTMINSTER MED SCH,DEPT ANAT,LONDON W6 8RF,ENGLAND
[2] TAN TOCK SENG HOSP,DEPT NEUROSURG,SINGAPORE 308433,SINGAPORE
关键词
calpain II; kainate; hippocampus;
D O I
10.1007/BF02454147
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The distributions of the kainate/DL-alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (KA/AMPA) receptors GluR1 and calcium-activated neutral protease II (calpain II) in the hippocampus of normal and kainate-lesioned rats were studied by immunocytochemistry. There was a reduction in GluR1 immunoreactivity and a slight increase in calpain II immunoreactivity on the dendrites of pyramidal neurons in CA fields affected by the kainate at 18 h postinjection. Calpain II immunoreactivity was associated with amyloid fibrils at electron microscopy. These fibrils were most often intracellular, in membrane-bound profiles, some of which were contacted by axon terminals and were identified as degenerating dendrites. There was extensive destruction of mitochondrial membranes in degenerating profiles, and accumulations of amyloid fibrils were often localised in mitochondria in a calpain-positive profile. This was unlike other, calpain-negative degenerating profiles, that contained tubulovesicular profiles or multilamellar bodies, where mitochondrial membranes were preserved. Many more calpain-positive profiles were observed at electron microscopy 6 days after kainate injection. The enzyme was present in macrophages and astrocytes in lesioned areas.
引用
收藏
页码:117 / 129
页数:13
相关论文
共 43 条
[1]   CALPAIN INHIBITORS IMPROVE THE RECOVERY OF SYNAPTIC TRANSMISSION FROM HYPOXIA IN HIPPOCAMPAL SLICES [J].
ARAI, A ;
KESSLER, M ;
LEE, K ;
LYNCH, G .
BRAIN RESEARCH, 1990, 532 (1-2) :63-68
[2]   PROTEOLYTIC-ENZYMES IN EXPERIMENTAL SPINAL-CORD INJURY [J].
BANIK, NL ;
HOGAN, EL ;
POWERS, JM ;
SMITH, KP .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1986, 73 (03) :245-256
[3]  
BELOCOPITOW E, 1965, J BIOL CHEM, V240, P3473
[4]   A SINGLE AMINO-ACID DETERMINES THE SUBUNIT-SPECIFIC SPIDER TOXIN BLOCK OF ALPHA-AMINO-3-HYDROXY-5-METHYLISOXAZOLE-4-PROPIONATE KAINATE RECEPTOR CHANNELS [J].
BLASCHKE, M ;
KELLER, BU ;
RIVOSECCHI, R ;
HOLLMANN, M ;
HEINEMANN, S ;
KONNERTH, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (14) :6528-6532
[5]   POLYCLONAL ANTISERA SPECIFIC FOR THE PROENZYME FORM OF EACH CALPAIN [J].
CROALL, DE ;
SLAUGHTER, CA ;
WORTHAM, HS ;
SKELLY, CM ;
DEOGNY, L ;
MOOMAW, CR .
BIOCHIMICA ET BIOPHYSICA ACTA, 1992, 1121 (1-2) :47-53
[6]   EXCITOTOXIC MECHANISMS IN THE PATHOGENESIS OF DEMENTIA [J].
DODD, PR ;
SCOTT, HL ;
WESTPHALEN, RI .
NEUROCHEMISTRY INTERNATIONAL, 1994, 25 (03) :203-219
[7]   CALPAIN ACTIVITY IN ORGANOPHOSPHORUS-INDUCED DELAYED NEUROPATHY (OPIDN) - EFFECTS OF A PHENYLALKYLAMINE CALCIUM-CHANNEL BLOCKER [J].
ELFAWAL, HAN ;
EHRICH, MF .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1993, 679 :325-329
[8]   CALCIUM INFLUX AND NEURODEGENERATION [J].
GIBBONS, SJ ;
BRORSON, JR ;
BLEAKMAN, D ;
CHARD, PS ;
MILLER, RJ .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1993, 679 :22-33
[9]   NEUROFILAMENT DISGUISE, DESTRUCTION AND DISCIPLINE [J].
GILBERT, DS ;
NEWBY, BJ ;
ANDERTON, BH .
NATURE, 1975, 256 (5518) :586-589
[10]   ALZHEIMERS-DISEASE AND DOWNS-SYNDROME - SHARING OF A UNIQUE CEREBROVASCULAR AMYLOID FIBRIL PROTEIN [J].
GLENNER, GG ;
WONG, CW .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1984, 122 (03) :1131-1135