Prenatal exposure to moderate levels of ethanol can have long-lasting effects on learning and memory in adult offspring

Citation
Rj. Sutherland et al., Prenatal exposure to moderate levels of ethanol can have long-lasting effects on learning and memory in adult offspring, PSYCHOBIOLO, 28(4), 2000, pp. 532-539
Citations number
45
Categorie Soggetti
Neurosciences & Behavoir
Journal title
PSYCHOBIOLOGY
ISSN journal
08896313 → ACNP
Volume
28
Issue
4
Year of publication
2000
Pages
532 - 539
Database
ISI
SICI code
0889-6313(200012)28:4<532:PETMLO>2.0.ZU;2-E
Abstract
Prenatal alcohol exposure can produce long-lasting cognitive and learning i mpairments in children. Previous studies have suggested that prenatal ethan ol exposure can produce neurochemical abnormalities in hippocampal formatio n. We examined whether performance in the Morris water task, known to be se nsitive to interference with hippocampal function, would be affected in adu lt offspring of rat darns who consumed moderate levels of ethanol through p regnancy. Rat darns consumed one of three diets throughout gestation: (1) B io-Serve liquid diet containing 5% ethanol (v/v; 26% EDC), which produces a maternal peak blood ethanol concentration of 100 mg/dl; (2) pair fed an is ocalorically equivalent amount of 0% ethanol liquid diet; or (3) laboratory chow ad Libitum. Adult offspring from each of the three maternal diet cond itions were brained in one of three versions of the Morris water task. We e mployed the "standard" fixed hidden platform task, the moving platform task , and a task that measures competition between cue and place navigation. Al l three groups learned to navigate normally in the fixed hidden platform ve rsion and showed clear preferences for the goal location during no-platform probe trials. In contrast, in the moving platform version and the cue vers us place competition task, the prenatally exposed rats were abnormal relati ve to the rats of the other two maternal diet conditions. In both of these tasks, they behaved in a manner consistent with the idea that acquisition o f new place information does not proceed as effectively as in normal rats. These data are consistent with the hypothesis that hippocampal circuitry an d neurochemistry related to synaptic plasticity are important targets under lying at least some of the long-lasting deleterious cognitive effects of pr enatal alcohol exposure.