CALBINDIN-D28K AND ISCHEMIC DAMAGE OF PYRAMIDAL CELLS IN RAT HIPPOCAMPUS

被引:53
作者
RAMI, A
RABIE, A
THOMASSET, M
KRIEGLSTEIN, J
机构
[1] UNIV MONTPELLIER 2, ENDOCRINOL NEUROBIOL LAB, CNRS, UA 1197, F-34060 MONTPELLIER, FRANCE
[2] INSERM, U20, F-78110 LE VESINET, FRANCE
关键词
ISCHEMIA; CALBINDIN-D28K; CALCIUM; RAT; HIPPOCAMPUS; VULNERABILITY;
D O I
10.1002/jnr.490310113
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
An antibody against rat calbindin-D28K, a calcium-binding protein present at high concentration in certain neurons of the central and peripheral nervous systems, was used to determine the progression of the pathological events in the rat hippocampus following experimental cerebral ischemia. Calbindin-D28K immunoreactivity is present in dentate granule cells and in the CA1-CA2 pyramidal cells. CA1 subfield contains a higher proportion of calbindin-D28K-positive pyramidal cells than does the CA2 subfield and CA1 cells are more immunoreactive than the CA2 cells. The pyramidal cells of the CA1 and CA2 subfields are vulnerable to ischemia. The cells in the CA1 became necrotic within 3-4 days after ischemia while those of the CA2 became necrotic within 2 days. There was a concomitant decrease in calbindin-D28K immunoreactivity in the whole hippocampal regio superior after ischemia which peaked 3 days postischemia. The difference in CA2 and CA1 vulnerability seemed to be inversely correlated with the calbindin-D28K contents of the CA2 and CA1 pyramidal cells. The decrease in the calbindin-D28K contents of these neurons was accompanied by cell damage. We therefore suggest that calbindin-D28K is an important factor for the survival of pyramidal cells in the hippocampal formation after ischemia.
引用
收藏
页码:89 / 95
页数:7
相关论文
共 38 条
[21]   NMDA-RECEPTOR ACTIVATION INCREASES CYTOPLASMIC CALCIUM-CONCENTRATION IN CULTURED SPINAL-CORD NEURONS [J].
MACDERMOTT, AB ;
MAYER, ML ;
WESTBROOK, GL ;
SMITH, SJ ;
BARKER, JL .
NATURE, 1986, 321 (6069) :519-522
[22]  
MONAGHAN DT, 1985, J NEUROSCI, V5, P2909
[23]   MAGNESIUM GATES GLUTAMATE-ACTIVATED CHANNELS IN MOUSE CENTRAL NEURONS [J].
NOWAK, L ;
BREGESTOVSKI, P ;
ASCHER, P ;
HERBET, A ;
PROCHIANTZ, A .
NATURE, 1984, 307 (5950) :462-465
[24]   TEMPORAL PROFILE OF NEURONAL DAMAGE IN A MODEL OF TRANSIENT FOREBRAIN ISCHEMIA [J].
PULSINELLI, WA ;
BRIERLEY, JB ;
PLUM, F .
ANNALS OF NEUROLOGY, 1982, 11 (05) :491-498
[26]   CHOLECALCIN (28-KDA CALCIUM-BINDING PROTEIN) IN THE RAT HIPPOCAMPUS - DEVELOPMENT IN NORMAL ANIMALS AND IN ALTERED THYROID STATES - AN IMMUNOCYTOCHEMICAL STUDY [J].
RAMI, A ;
BREHIER, A ;
THOMASSET, M ;
RABIE, A .
DEVELOPMENTAL BIOLOGY, 1987, 124 (01) :228-238
[27]   THE COMPARATIVE IMMUNOCYTOCHEMICAL DISTRIBUTION OF 28 KDA CHOLECALCIN (CABP) IN THE HIPPOCAMPUS OF RAT, GUINEA-PIG AND HEDGEHOG [J].
RAMI, A ;
BREHIER, A ;
THOMASSET, M ;
RABIE, A .
BRAIN RESEARCH, 1987, 422 (01) :149-153
[28]  
SIESJO BK, 1988, ANN NY ACAD SCI, V522, P638
[29]   CELL-DAMAGE IN THE BRAIN - A SPECULATIVE SYNTHESIS [J].
SIESJO, BK .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1981, 1 (02) :155-185
[30]   CALCIUM OVERLOAD IN SELECTIVELY VULNERABLE NEURONS OF THE HIPPOCAMPUS DURING AND AFTER ISCHEMIA - AN ELECTRON-MICROSCOPY STUDY IN THE RAT [J].
SIMON, RP ;
GRIFFITHS, T ;
EVANS, MC ;
SWAN, JH ;
MELDRUM, BS .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1984, 4 (03) :350-361