Abstract
Prenatal exposure to high levels of alcohol is strongly associated with poor cognitive outcomes particularly in relation to learning and memory. It is also becoming more evident that anxiety disorders and anxiety-like behaviour can be associated with prenatal alcohol exposure. This study used a rat model to determine if prenatal exposure to a relatively small amount of alcohol would result in anxiety-like behaviour and to determine if this was associated with morphological changes in the basolateral amygdala. Pregnant Sprague Dawley rats were fed a liquid diet containing either no alcohol (Control) or 6% (vol/vol) ethanol (EtOH) throughout gestation. Male and Female offspring underwent behavioural testing at 8 months (Adult) or 15 months (Aged) of age. Rats were perfusion fixed and brains were collected at the end of behavioural testing for morphological analysis of pyramidal neuron number and dendritic morphology within the basolateral amygdala. EtOH exposed offspring displayed anxiety-like behaviour in the elevated plus maze, holeboard and emergence tests. Although sexually dimorphic behaviour was apparent, sex did not impact anxiety-like behaviour induced by prenatal alcohol exposure. This increase in anxiety – like behaviour could not be attributed to a change in pyramidal cell number within the BLA but rather was associated with an increase in dendritic spines along the apical dendrite which is indicative of an increase in synaptic connectivity and activity within these neurons. This study is the first to link increases in anxiety like behaviour to structural changes within the basolateral amygdala in a model of prenatal ethanol exposure. In addition, this study has shown that exposure to even a relatively small amount of alcohol during development leads to long term alterations in anxiety-like behaviour.
Highlights
Consumption of alcohol during pregnancy can be detrimental to the healthy development of the fetus as well as continued growth and development after birth
There were no significant differences in maternal diet consumption, weight gain, gestation length or litter size between dams fed an ethanol containing diet (EtOH) and dams fed an isocaloric control diet (Control)
Our low dose prenatal ethanol exposed animals exhibited a clear but subtle phenotype for anxiety-like behaviour in the Elevated Plus Maze (EPM), holeboard, and emergence tests, which was present in both adult and aged animals
Summary
Consumption of alcohol during pregnancy can be detrimental to the healthy development of the fetus as well as continued growth and development after birth. Consumption of large amounts of alcohol during pregnancy often results in a specific pattern of facial, cranial and cerebral malformations and mental retardation in the offspring known as fetal alcohol syndrome (FAS) [3,4,5,6,7,8]. FAS is the most severe outcome in a broad spectrum of cognitive and behavioural effects associated with fetal alcohol exposure collectively grouped under the umbrella term fetal alcohol spectrum disorders (FASD) [9,10,11,12] These poor cognitive outcomes can include difficulties with learning and memory [4,13,14,15,16,17,18,19], social interaction and engagement [20,21], hyperactivity and attention [4,10,20]. Many of these problems are most prominent during schooling but can often persist well into and throughout adulthood [4,22,23,24]
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