QUANTITATIVE-ANALYSIS OF THE ELECTROCORTICOGRAM AFTER FOREBRAIN ISCHEMIA IN THE RAT

被引:15
作者
PERUCHE, B [1 ]
KLAASSENS, H [1 ]
KRIEGLSTEIN, J [1 ]
机构
[1] UNIV MARBURG,INST PHARMAKOL & TOXIKOL,FACHBEREICH PHARM & LEBENSMITTELCHEM,D-35032 MARBURG,GERMANY
关键词
BRAIN; ELECTROCORTICOGRAM; ISCHEMIA; PHENCYCLIDINE; NEURONAL DAMAGE;
D O I
10.1159/000139287
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The purpose of the study was to test the hypothesis that the postischemic neuronal damage is accompanied by changes of the electrocorticogram (ECoG) of freely moving rats during long-term recovery after forebrain ischemia. Ten minutes forebrain ischemia was induced in male Wistar rats. ECoG was recorded 1 day before as well as 1 h, 1 day and 7 days after ischemia. The ECoG power was calculated and for characterizing postischemic ECoG development the percentage of preischemic ECoG power was evaluated. The awake state of the rats was considered for analysis only. Furthermore, the neuroprotective effect of phencyclidine (PCP, 5 mg/kg i.v., 15 min prior to ischemia) was demonstrated in the ECoG changes. One hour after ischemia the ECoG power of the theta (4.75-6.75 Hz), alpha (7.00-12.50 Hz) and beta (12.75-18.50 Hz) band was decreased compared with sham-operated controls and PCP did not influence these changes. However, I day after ischemia ECoG power of the saline-treated ischemic rats was completely restored and no longer different from that of the sham-operated group. PCP-treated ischemic animals showed significantly elevated ECoG power in comparison with saline-treated animals. Seven days after ischemia ECoG power of the saline-treated ischemic rats again decreased. In comparison with the ischemic controls, the ECoG activity of the PCP-treated ischemic rats was significantly higher. PCP maintained postischemic ECoG power at the non-ischemic control level. It is suggested that the decrease in the ECoG activity several days after ischemia is related to the delayed neuronal damage. PCP is known to protect neurons against this ischemic damage and, therefore, ECoG activity in PCP-treated rats is less reduced than in untreated controls.
引用
收藏
页码:229 / 237
页数:9
相关论文
共 34 条
[1]   BEHAVIORAL, ELECTROENCEPHALOGRAPHIC AND HISTOPATHOLOGICAL STUDIES ON MONGOLIAN GERBILS WITH OCCLUDED COMMON CAROTID ARTERIES [J].
ARAKI, H ;
NOJIRI, M ;
KAWASHIMA, K ;
KIMURA, M ;
AIHARA, H .
PHYSIOLOGY & BEHAVIOR, 1986, 38 (01) :89-94
[2]   ELEVATION OF THE EXTRACELLULAR CONCENTRATIONS OF GLUTAMATE AND ASPARTATE IN RAT HIPPOCAMPUS DURING TRANSIENT CEREBRAL-ISCHEMIA MONITORED BY INTRACEREBRAL MICRODIALYSIS [J].
BENVENISTE, H ;
DREJER, J ;
SCHOUSBOE, A ;
DIEMER, NH .
JOURNAL OF NEUROCHEMISTRY, 1984, 43 (05) :1369-1374
[3]  
BUZSAKI G, 1989, EXP BRAIN RES, V78, P268
[4]   GLUTAMATE NEUROTOXICITY AND DISEASES OF THE NERVOUS-SYSTEM [J].
CHOI, DW .
NEURON, 1988, 1 (08) :623-634
[5]   CELLULAR-ORIGIN OF ISCHEMIA-INDUCED GLUTAMATE RELEASE FROM BRAIN-TISSUE INVIVO AND INVITRO [J].
DREJER, J ;
BENVENISTE, H ;
DIEMER, NH ;
SCHOUSBOE, A .
JOURNAL OF NEUROCHEMISTRY, 1985, 45 (01) :145-151
[6]   POSTISCHEMIC ALTERATIONS OF SPONTANEOUS ACTIVITIES IN RAT HIPPOCAMPAL CA1-NEURONS [J].
FURUKAWA, K ;
YAMANA, K ;
KOGURE, K .
BRAIN RESEARCH, 1990, 530 (02) :257-260
[7]  
GOLDBERG MP, 1988, J PHARMACOL EXP THER, V245, P1081
[8]   AUTOMATIC-ANALYSIS OF SLEEP-WAKING CYCLE IN RAT RECORDED BY MINIATURE TELEMETRY [J].
GOTTESMANN, C ;
KIRKHAM, PA ;
LACOSTE, G ;
RODRIGUES, L ;
ARNAUD, C .
BRAIN RESEARCH, 1977, 132 (03) :562-568
[9]   ISCHEMIA-INDUCED SHIFT OF INHIBITORY AND EXCITATORY AMINO-ACIDS FROM INTRACELLULAR TO EXTRACELLULAR COMPARTMENTS [J].
HAGBERG, H ;
LEHMANN, A ;
SANDBERG, M ;
NYSTROM, B ;
JACOBSON, I ;
HAMBERGER, A .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1985, 5 (03) :413-419
[10]   DELAYED NEURONAL DEATH IS INDUCED WITHOUT POSTISCHEMIC HYPEREXCITABILITY - CONTINUOUS MULTIPLE-UNIT RECORDING FROM ISCHEMIC CA1 NEURONS [J].
IMON, H ;
MITANI, A ;
ANDOU, Y ;
ARAI, T ;
KATAOKA, K .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1991, 11 (05) :819-823