Neuroanatomical and neurophysiological mechanisms involved in central nervous system dysfunctions induced by prenatal alcohol exposure

被引:153
作者
Guerri, C [1 ]
机构
[1] Inst Invest Citological Caja Ahorros Valencia, Valencia 46010, Spain
关键词
prenatal ethanol exposure; alcohol; brain development; neocortex; hippocampus;
D O I
10.1111/j.1530-0277.1998.tb03653.x
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
One of the most severe consequences of maternal ethanol consumption is:he damage to the developing central nervous system, which is manifested by long-term cognitive and behavioral deficits in the offspring. Prenatal exposure to ethanol affects many crucial neurochemical and cellular components of the developing brain. Ethanol interferes with all of the stages of brain development, and the severity of the damage depends on the amount of ethanol intake and level of exposure. Experimental observations also indicate that the toxic effects of ethanol are not uniform: some brain regions are more affected than others and, even within a given region, same cell populations are more vulnerable than others. The neocortex, the hippocampus, and the cerebellum are the regions in which the neurotoxic effects of ethanol have been associated with the behavioral deficits. At the cellular level, ethanol disrupts basic developmental processes, including interference with division and proliferation, cell growth, and differentiation and the migration of maturing cells, Alterations in astroglia development and In neuronal-glial interactions may also influence the development of the nervous system, An impairment of several neurotransmitter systems and/or their receptors, as well as changes in the endocrine environment during brain development, are also important factors involved in the behavioral dysfunctions observed after prenatal ethanol exposure. Finally, some molecular mechanisms of ethanol-induced behavioral dysfunctions will be discussed.
引用
收藏
页码:304 / 312
页数:9
相关论文
共 101 条
[1]   MATERNAL RISK-FACTORS IN FETAL-ALCOHOL-SYNDROME - PROVOCATIVE AND PERMISSIVE INFLUENCES [J].
ABEL, EL ;
HANNIGAN, JH .
NEUROTOXICOLOGY AND TERATOLOGY, 1995, 17 (04) :445-462
[2]   ALCOHOL PRODUCES SPASMS OF HUMAN UMBILICAL BLOOD-VESSELS - RELATIONSHIP TO FETAL ALCOHOL SYNDROME (FAS) [J].
ALTURA, BM ;
ALTURA, BT ;
CARELLA, A ;
CHATTERJEE, M ;
HALEVY, S ;
TEJANI, N .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1982, 86 (02) :311-312
[3]  
Baek JK, 1996, MOL BRAIN RES, V40, P161
[4]   PRENATAL ETHANOL EXPOSURE PERMANENTLY REDUCES THE NUMBER OF PYRAMIDAL NEURONS IN RAT HIPPOCAMPUS [J].
BARNES, DE ;
WALKER, DW .
DEVELOPMENTAL BRAIN RESEARCH, 1981, 1 (03) :333-340
[5]   NEONATAL ALCOHOL EXPOSURE ALTERS SUCKLING BEHAVIOR IN NEONATAL RAT PUPS [J].
BARRON, S ;
KELLY, SJ ;
RILEY, EP .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1991, 39 (02) :423-427
[6]   EFFECT OF ETHANOL CHRONICALLY ADMINISTERED TO PREWEANLING RATS ON CEREBELLAR DEVELOPMENT - MORPHOLOGICAL-STUDY [J].
BAUERMOFFETT, C ;
ALTMAN, J .
BRAIN RESEARCH, 1977, 119 (02) :249-268
[7]   ALCOHOL-INDUCED NEURONAL LOSS IN DEVELOPING RATS - INCREASED BRAIN-DAMAGE WITH BINGE EXPOSURE [J].
BONTHIUS, DJ ;
WEST, JR .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1990, 14 (01) :107-118
[8]   PERMANENT NEURONAL DEFICITS IN RATS EXPOSED TO ALCOHOL DURING THE BRAIN GROWTH SPURT [J].
BONTHIUS, DJ ;
WEST, JR .
TERATOLOGY, 1991, 44 (02) :147-163
[9]   EFFECTS OF ETHANOL ON POSTNATAL CELL ACQUISITION IN THE RAT CEREBELLUM [J].
BORGES, S ;
LEWIS, PD .
BRAIN RESEARCH, 1983, 271 (02) :388-391
[10]   Free radicals and ethanol-induced cytotoxicity in neural crest cells [J].
Chen, SY ;
Sulik, KK .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1996, 20 (06) :1071-1076