Alcohol exposure (AE) during pregnancy is known to affect fetal medial prefrontal cortex (mPFC) and hippocampus (HC) development. Previous work has demonstrated that these two structures are vulnerable to AE during the brain growth spurt, which occurs during 3rd trimester of human pregnancy and the first two postnatal weeks in rodents. Our lab has shown that thalamic nucleus reuniens (Re) is damaged in a rodent model of human 3rd trimester AE. We have also shown that Re is critical for mPFC–HC oscillatory synchrony and spatial working memory (SWM). The current study investigated the effects of early AE on SWM ability in adulthood in rats. We predicted that AE would lead to SWM impairment that worsened as working memory demand increased. We administered 5.25 g/kg/day of ethanol in milk formula via intragastric intubations in a binge manner on PD 4-9 (AE group) or performed intubations without liquid (sham intubated (SI) group). On PD90, rats were trained on a continuous alternation (CA) T-maze task. Upon reaching a choice accuracy criterion of 80% for two consecutive days on CA, we introduced a delay between trials (DA) in order to increase SWM demand. The rats underwent 6 DA sessions, consisting of 12 each of 10-second (s), 30 s, and 60 s delay trials given in a pseudorandom sequence. Our results show that animals in both AE and SI groups learned the CA task at similar rates. However, on the DA task, the SI group showed consistent improvement across sessions on the 30-s delay trials, whereas the AE group did not (postnatal - treatment x day interaction: F(5,195)=2.70, p = .02). For the 10 s delay trials, both AE and SI groups showed improvement across days (main effect of day: F(5,195)=7.93 , p < .001), whereas for the 60 s delay trials, both groups performed uniformly poorly across days. These findings support the hypothesis that binge AE during the brain growth spurt produces SWM deficits that depend on SWM demand. This study will lead to a better understanding of the impact of HC-Re-mPFC circuitry damage due to developmental AE on cognitive function later in life.

Delay-dependent spatial working memory deficits in a rat model of third trimester alcohol exposure.

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Delay-dependent spatial working memory deficits in a rat model of third trimester alcohol exposure.

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