Effects of prenatal alcohol exposure on the hippocampus: Spatial behavior, electrophysiology, and neuroanatomy

Abstract

Prenatal exposure to alcohol can result in fetal alcohol syndrome (FAS), characterized by growth retardation, facial dysmorphologies, and a host of neurobehavioral impairments. Neurobehavioral effects in FAS, and in alcohol‐related neurodevelopmental disorder, include poor learning and memory, attentional deficits, and motor dysfunction. Many of these behavioral deficits can be modeled in rodents. This paper reviews the literature suggesting that many fetal alcohol effects result, at least in part, from teratogenic effects of alcohol on the hippocampus. Neurobehavioral studies show that animals exposed prenatally to alcohol are impaired in many of the same spatial learning and memory tasks sensitive to hippocampal damage, including T‐mazes, the Morris water maze, and the radial arm maze. Direct evidence for hippocampal involvement is provided by neuroanatomical studies of the hippocampus documenting reduced numbers of neurons, lower dendritic spine density on pyramidal neurons, and decreased morphological plasticity after environmental enrichment in rats exposed prenatally to alcohol. Electrophysiological studies also demonstrate changes in synaptic activity in in vitro hippocampal brain slices isolated from prenatal alcohol‐exposed animals. Considered together, these observations demonstrate that prenatal exposure to alcohol can result in abnormal hippocampal development and function. Such studies provide a better understanding of neurological deficits associated with FAS in humans, and may also contribute to the development of strategies to ameliorate the effects of prenatal alcohol exposure on behavior. Hippocampus 2000;10:94–110. © 2000 Wiley‐Liss, Inc.

Ethanol–BDNF interactions: Still more questions than answers

“…Rodents exposed to ethanol in utero or during the early postnatal period (a period roughly equivalent to the third trimester of human development) display microcephaly, hyperactivity, reduced cerebellar Purkinje cells, ataxia and learning deficits, which are also hallmarks of the human disorder (reviewed by Berman and Hannigan, 2000;Burn et al, 2003). The striking similarities between FASD models and BDNF haplodeficient mice suggest that the two phenotypes may be developmentally linked.…”

Immature hippocampal neuronal networks do not develop tolerance to the excitatory actions of ethanol

“…Keywords chronic; GABA; excitatory; depolarizing; network; fetal Numerous animal and human studies have demonstrated that EtOH (ethanol) exposure damages the developing hippocampus, leading to deficits in learning and memory (Berman & Hannigan, 2000;Bonthius et al, 2001a;Bonthius et al, 2001b;Mattson et al, 2001;Hamilton et al, 2003). These deficits are a consequence of structural and functional hippocampal abnormalities that persist into adulthood (Sutherland et al, 1997;Krahl et al, 1999;Berman & Hannigan, 2000;Richardson et al, 2002;Savage et al, 2002). Multiple candidate mechanisms could be responsible for these effects of EtOH, including alterations in cellular energetics, gene expression, cell-cell interactions, cell signaling pathways and synaptic Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication.…”

Cortical Synaptogenesis in the Human Brain in Conditions of Prenatal Alcoholization

“…The consequence of this was the "thinning" of the structure of elementary membranes and damaged membranes are less able to establish close contacts with each other, which is probably also connected with reduced ability of cells that are in constant contact with ethanol, synthesize neurotransmitters, which fill the synaptic vesicles [14]. This greatly disturbed neuronal mechanisms underlying the susceptibility and processing of information, which in turn may adversely affect the mental activity of the individual.…”