Intrauterine methylmercury intoxication - Consequence of the inherent brain lesions and cognitive dysfunction in maturity

被引:44
作者
Kakita, A
Wakabayashi, K
Su, M
Yoneoka, Y
Sakamoto, M
Ikuta, F
Takahashi, H
机构
[1] Niigata Univ, Brain Res Inst, Dept Pathol, Niigata 9518585, Japan
[2] Niigata Univ, Brain Res Inst, Brain Dis Res Ctr, Niigata 9518585, Japan
[3] Niigata Univ, Brain Res Inst, Dept Neurosurg, Niigata 9518585, Japan
[4] Natl Inst Minamata Dis, Dept Epidemiol, Kumamoto 8670008, Japan
[5] Niigata Neurosurg Hosp & Brain Res Ctr, Niigata 9501101, Japan
关键词
methylmercury; intrauterine neurotoxicity; fetal-type minamata disease; memory formation;
D O I
10.1016/S0006-8993(00)02717-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We studied the effects of intrauterine neurotoxicity by methylmercury (MeHg) on the postnatal developing and adult stages of rats. We used offspring delivered from darns that had been given 1 mg/kg/day methylmercury chloride for 5 pregestational days and throughout pregnancy. Histopathological examination of the brains of a proportion of the offspring on postnatal days 1 (P1) and P3 revealed degenerative neurons in the brain stem and the limbic system, including the hippocampus and the amygdala. At P7 and P14, degenerative neurons were indiscemible. but reactive astrocytosis remained in the brain stem. Ar P70 and P180, the brains seemed to have developed well. However, in behavioral analyses performed at 6 months of age, MeHg-exposed rats showed a significant learning disability in the passive avoidance response compared with controls, but no differences in water maze performance. Furthermore, morphometric analysis of the amygdala and hippocampus revealed significantly fewer neurons in both areas in the MeHg-exposed rats. Thus, chronic intrauterine exposure to low-dose MeHg induces a decrease in neuron population in the Limbic system, and the offspring have impaired higher brain function. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:322 / 330
页数:9
相关论文
共 51 条
[1]  
AMINZAKI L, 1974, PEDIATRICS, V54, P587
[2]  
BAYER SA, 1993, NEUROTOXICOLOGY, V14, P83
[3]  
Berlin M., 1986, Handbook of the Toxicology of Metals, P387
[4]   OPERANT-BEHAVIOR PERFORMANCE CHANGES IN RATS AFTER PRENATAL METHYLMERCURY EXPOSURE [J].
BORNHAUSEN, M ;
MUSCH, HR ;
GREIM, H .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1980, 56 (03) :305-310
[5]   THE EFFECTS OF METHYLMERCURY ON THE DEVELOPING BRAIN [J].
CHOI, BH .
PROGRESS IN NEUROBIOLOGY, 1989, 32 (06) :447-470
[6]   ABNORMAL NEURONAL MIGRATION, DERANGED CEREBRAL CORTICAL ORGANIZATION, AND DIFFUSE WHITE MATTER ASTROCYTOSIS OF HUMAN FETAL BRAIN - MAJOR EFFECT OF METHYLMERCURY POISONING INUTERO [J].
CHOI, BH ;
LAPHAM, LW ;
AMINZAKI, L ;
SALEEM, T .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1978, 37 (06) :719-733
[7]   Brain lesions and delayed water maze learning deficits after intracerebroventricular spermine [J].
Conway, EL .
BRAIN RESEARCH, 1998, 800 (01) :10-20
[8]  
Davidson PW, 1995, NEUROTOXICOLOGY, V16, P677
[9]   METHYLMERCURY POISONING - LONG-TERM CLINICAL, RADIOLOGICAL, TOXICOLOGICAL, AND PATHOLOGICAL-STUDIES OF AN AFFECTED FAMILY [J].
DAVIS, LE ;
KORNFELD, M ;
MOONEY, HS ;
FIEDLER, KJ ;
HAALAND, KY ;
ORRISON, WW ;
CERNICHIARI, E ;
CLARKSON, TW .
ANNALS OF NEUROLOGY, 1994, 35 (06) :680-688
[10]  
ENGLESSON G, 1952, ACTA PAEDIATR, V441, P289