CALBINDIN-D28K-CONTAINING NEURONS IN ANIMAL-MODELS OF NEURODEGENERATION - POSSIBLE PROTECTION FROM EXCITOTOXICITY

被引:183
作者
IACOPINO, A
CHRISTAKOS, S
GERMAN, D
SONSALLA, PK
ALTAR, CA
机构
[1] UNIV MED & DENT NEW JERSEY,DEPT BIOCHEM & MOLEC BIOL,NEWARK,NJ 07103
[2] UNIV TEXAS,SW MED CTR,DEPT PSYCHIAT,DALLAS,TX 75230
[3] UNIV MED & DENT NEW JERSEY,DEPT NEUROL,PISCATAWAY,NJ 08903
[4] REGENERON PHARMACEUT INC,TARRYTOWN,NY 10591
来源
MOLECULAR BRAIN RESEARCH | 1992年 / 13卷 / 03期
关键词
CALBINDIN-D28K; NEURODEGENERATION; MPTP; EXCITOTOXIN; NEUROPROTECTION; ANIMAL MODEL; IMMUNOCYTOCHEMISTRY;
D O I
10.1016/0169-328X(92)90033-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Brain levels of the calcium binding protein Calbindin-D28K (CaBP28K) and CaBP28K mRNA were measured for various animal models of neurodegenerative diseases (MPTP-treated C57BL/6J mice and Sprague-Dawley rats receiving striatal/intraperitoneal kainic acid or quinolinic acid into the nucleus basalis magnocellularis). Brain areas were tested (radioimmunoassay, Western blot, slot blot, and Northern blot) for levels of CaBP28K and CaBP28K mRNA. The various models did not exhibit any changes in protein or mRNA levels from the controls, suggesting that CaBP28K-containing neurons were not lost after exposure to these neurotoxins. Immunocytochemical characterization of the substantia nigra of the MPTP-treated mice revealed that there was significant dopaminergic cell loss in this brain area after MPTP treatment. The majority of dopaminergic neurons that degenerated did not contain CaBP28K. The small percentage of surviving neurons were CaBP28K-positive. These results suggest that the presence of CaBP28K may protect neurons from calcium-mediated neurotoxicity.
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页码:251 / 261
页数:11
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