COEXPRESSION OF HSP72 AND C-FOS IN RAT-BRAIN FOLLOWING KAINIC ACID TREATMENT

被引:41
作者
SCHREIBER, SS [1 ]
NAJM, I [1 ]
TOCCO, G [1 ]
BAUDRY, M [1 ]
机构
[1] UNIV SO CALIF,NEUROSCI PROGRAM,LOS ANGELES,CA 90089
关键词
HEAT SHOCK PROTEIN; C-FOS; KAINIC ACID; NEURODEGENERATION; GENE EXPRESSION; IMMUNOCYTOCHEMISTRY; IN SITU HYBRIDIZATION;
D O I
10.1097/00001756-199312000-00022
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
THE relationship between heat shock protein 72 (HSP72) and c-fos gene expression following systemic administration of kainic acid was investigated by combining immunocytochemistry for HSP72 with in situ hybridization for c-fos. Increased HSP72 expression was detected in adult rat hippocampus 4 h after seizure-onset. Transient coexpression of c-fos and HSP72 occurred in neurons that are resistant to kainic acid, whereas prolonged coexpression was observed in vulnerable neurons. The spatial distribution and developmental time course of kainic acid-induced HSP72 expression were similar to those of kainic acid-induced neurodegeneration. The results demonstrate a relationship between c-fos and HSP72 gene expression and suggest that prolonged co-expression of these genes plays a role in kainic acid-induced neuronal death.
引用
收藏
页码:269 / 272
页数:4
相关论文
共 25 条
  • [1] TEMPORAL PROFILE OF THE INDUCTION OF HEAT-SHOCK PROTEIN-70 AND HEAT-SHOCK COGNATE PROTEIN-70 MESSENGER-RNAS AFTER TRANSIENT ISCHEMIA IN GERBIL BRAIN
    AOKI, M
    ABE, K
    KAWAGOE, J
    SATO, S
    NAKAMURA, S
    KOGURE, K
    [J]. BRAIN RESEARCH, 1993, 601 (1-2) : 185 - 192
  • [2] HYPERTHERMIA PROTECTS AGAINST LIGHT DAMAGE IN THE RAT RETINA
    BARBE, MF
    TYTELL, M
    GOWER, DJ
    WELCH, WJ
    [J]. SCIENCE, 1988, 241 (4874) : 1817 - 1820
  • [3] INDUCTION OF A HEAT-SHOCK GENE AT THE SITE OF TISSUE-INJURY IN THE RAT-BRAIN
    BROWN, IR
    RUSH, S
    IVY, GO
    [J]. NEURON, 1989, 2 (06) : 1559 - 1564
  • [4] TRANSIENT HYPERTHERMIA PROTECTS AGAINST SUBSEQUENT FOREBRAIN ISCHEMIC CELL-DAMAGE IN THE RAT
    CHOPP, M
    CHEN, H
    HO, KL
    DERESKI, MO
    BROWN, E
    HETZEL, FW
    WELCH, KMA
    [J]. NEUROLOGY, 1989, 39 (10) : 1396 - 1398
  • [5] HYPOXIA ISCHEMIA INDUCES HEAT-SHOCK PROTEIN-LIKE (HSP72) IMMUNOREACTIVITY IN NEONATAL RAT-BRAIN
    FERRIERO, DM
    SOBERANO, HQ
    SIMON, RP
    SHARP, FR
    [J]. DEVELOPMENTAL BRAIN RESEARCH, 1990, 53 (01): : 145 - 150
  • [6] HEAT-SHOCK PROTEINS AS MARKERS OF NEURAL INJURY
    GONZALEZ, MF
    SHIRAISHI, K
    HISANAGA, K
    SAGAR, SM
    MANDABACH, M
    SHARP, FR
    [J]. MOLECULAR BRAIN RESEARCH, 1989, 6 (01): : 93 - 100
  • [7] COMPETITIVE-INHIBITION OF HSP70 GENE-EXPRESSION CAUSES THERMOSENSITIVITY
    JOHNSTON, RN
    KUCEY, BL
    [J]. SCIENCE, 1988, 242 (4885) : 1551 - 1554
  • [8] ISCHEMIC TOLERANCE PHENOMENON FOUND IN THE BRAIN
    KITAGAWA, K
    MATSUMOTO, M
    TAGAYA, M
    HATA, R
    UEDA, H
    NIINOBE, M
    HANDA, N
    FUKUNAGA, R
    KIMURA, K
    MIKOSHIBA, K
    KAMADA, T
    [J]. BRAIN RESEARCH, 1990, 528 (01) : 21 - 24
  • [9] HEAT-SHOCK RESISTANCE CONFERRED BY EXPRESSION OF THE HUMAN HSP27 GENE IN RODENT CELLS
    LANDRY, J
    CHRETIEN, P
    LAMBERT, H
    HICKEY, E
    WEBER, LA
    [J]. JOURNAL OF CELL BIOLOGY, 1989, 109 (01) : 7 - 15
  • [10] DISTRIBUTION OF THE 72-KD HEAT-SHOCK PROTEIN AS A FUNCTION OF TRANSIENT FOCAL CEREBRAL-ISCHEMIA IN RATS
    LI, Y
    CHOPP, M
    GARCIA, JH
    YOSHIDA, Y
    ZHANG, ZG
    LEVINE, SR
    [J]. STROKE, 1992, 23 (09) : 1292 - 1298