Electro-cortical signs of early neuronal damage following transient global cerebral ischemia in rat

被引:8
作者
Moldovan, M
Zagrean, AM
Avrameseu, S
Savaran, V
Zagrean, L
机构
[1] Carol Davila Univ Med & Pharm, Dept Physiol, Fac Med, Bucharest 76241, Romania
[2] Univ Copenhagen, Panum Inst, Div Neurophysiol, Inst Med Physiol, Copenhagen, Denmark
来源
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | 2004年 / 8卷 / 01期
关键词
global cerebral ischemia; ECoG; burst-suppression;
D O I
10.1111/j.1582-4934.2004.tb00268.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
During recovery after a transient global cerebral ischemia (TGCI), rat electrocorticogam (ECoG) shows epochs of synchronized activity (SA) alternating with epochs of low amplitude background activity (BA). The aim of this study was to compare the changes in these electrical activities during a 30-min recovery period that followed either a non-injuring (3 minutes, N=10) or an injuring (10 minutes, N=10) TGCI. During TGCI there was a 3 fold reduction n amplitudes of both SA and BA but no changes in frequency. During reperfusion following a 3 minutes TGCI, the amplitudes of both SA and BA recovered to about 70%. During the reperfusion that followed a 10 minutes TGCI, BA showed no recovery, whereas SA recovered to about 40%. During the 30 min reperfusion, there was a time-dependent decrease in the frequency of SA, but independent on the duration of TGCI. In contrast, the frequency of the BA did not change during reperfusion. Our data indicate that following cerebral ischemia the recovery of SA cm take place independently of BA. The lack of recovery in BA may indicate early subcortical neuronal damage.
引用
收藏
页码:135 / 140
页数:6
相关论文
共 16 条
[1]  
GAIN E A, 1957, Can Anaesth Soc J, V4, P289
[2]   Neurological recovery by EEG bursting after resuscitation from cardiac arrest in rats [J].
Geocadin, RG ;
Sherman, DL ;
Hansen, HC ;
Kimura, T ;
Niedermeyer, E ;
Thakor, NV ;
Hanley, DF .
RESUSCITATION, 2002, 55 (02) :193-200
[3]   Early electrophysiological and histologic changes after global cerebral ischemia in rats [J].
Geocadin, RG ;
Muthuswamy, J ;
Sherman, DL ;
Thakor, NV ;
Hanley, DF .
MOVEMENT DISORDERS, 2000, 15 :14-21
[4]   FUNCTIONAL AND MORPHOLOGICAL-CHANGES INDUCED BY TRANSIENT IN-VIVO ISCHEMIA [J].
HORI, N ;
CARPENTER, DO .
EXPERIMENTAL NEUROLOGY, 1994, 129 (02) :279-289
[5]  
Moldovan M, 1998, Rom J Physiol, V35, P33
[6]  
MOLDOVAN M, 2000, J MED BIOCH, V4, P103
[7]   The burst-suppression electroencephalogram [J].
Niedermeyer, E ;
Sherman, DL ;
Geocadin, RJ ;
Hansen, HC ;
Hanley, DF .
CLINICAL ELECTROENCEPHALOGRAPHY, 1999, 30 (03) :99-105
[8]   Oxidative damage following cerebral ischemia depends on reperfusion - a biochemical study in rat [J].
Nita, DA ;
Nita, V ;
Spulber, S ;
Moldovan, M ;
Popa, DP ;
Zagrean, AM ;
Zagrean, L .
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2001, 5 (02) :163-170
[9]   NEW MODEL OF BILATERAL HEMISPHERIC ISCHEMIA IN THE UNANESTHETIZED RAT [J].
PULSINELLI, WA ;
BRIERLEY, JB .
STROKE, 1979, 10 (03) :267-272
[10]   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