Effect of developmental alcohol exposure on the structure and function of the medial prefrontal cortical-reuniens-hippocampal circuit in a rodent model of fetal alcohol spectrum disorders
Date
2023
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Publisher
University of Delaware
Abstract
Fetal Alcohol Spectrum Disorders encompass an array of developmental disorders defined by physical, behavioral, and cognitive deficits as a result of prenatal exposure to alcohol. As many as 1 in 20 live births in the United States have been exposed to sufficient alcohol exposure to produce lasting, significant impairments in these areas. Among these deficits, a notable effect of AE is damage seen to executive function, a set of cognitive controls involved in goal-directed behaviors. Executive function regulation has been associated with activity in both the hippocampus and medial prefrontal cortex in the mammalian brain. However, an intermediary structure, the nucleus reuniens has been implicated in the reciprocal communication between the hippocampus and medial prefrontal cortex. Research has demonstrated that developmental AE can specifically damage the reuniens, compromising signal transmission between structures. It is therefore hypothesized that damage to the structural integrity of the medial prefrontal cortical-reuniens-hippocampal circuit is linked to executive function deficits observed in Fetal Alcohol Spectrum Disorders by compromising synchrony between the medial prefrontal cortex and hippocampus. ☐ This study used a rodent model of third trimester binge alcohol exposure to examine the neuroanatomical alterations to the reuniens that result from neonatal alcohol exposure and linking these findings to previous work that used an associative memory behavioral task to model executive function. This study examined the effects of developmental alcohol exposure on neuron activation and loss of neurons in the nucleus reuniens. It was expected, and found, that neonatal alcohol exposure significantly reduced the number of mature neurons, as well as the number of activated mature neurons in the reuniens. It was expected that activation of other non-neuronal cells would be negatively affected, however we did not find an effect of alcohol exposure on activation of non-neuronal cell types. This finding suggests that anatomical alterations to the reuniens may play a major role in executive dysfunction observed in Fetal Alcohol Spectrum Disorders.
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Keywords
Executive function, FASD, Fetal Alcohol Spectrum Disorders, Nucleus reuniens, Developmental disorders