Description
Alcohol exposure can interfere with prenatal development. The term fetal alcohol spectrum disorders (FASD) refers to the range of detrimental outcomes associated with prenatal alcohol exposure (PAE). Attention deficits are a hallmark feature of FASD, and these children are commonly treated with methylphenidate. Research is mixed regarding effectiveness of methylphenidate treatment for FASD. Along with neurobehavioral deficits, PAE can lead to secondary disabilities including substance use problems. It’s hypothesized that, compared to controls, mice with PAE will: be more prone to the development of locomotor sensitization following repeated methylphenidate treatment (Aim1); consume more alcohol than controls in a binge-like drinking paradigm (Aim2a); and consume more alcohol as a function of prior methylphenidate treatment (Aim2b). Pregnant C57B6xFVB/NJF1 hybrid female mice were provided access to 20% EtOH or vehicle from gestational day 7-16. The F2 hybrid offspring were evaluated for locomotor responses to methylphenidate and alcohol intake. Testing began on postnatal day (PND)35. Aim 1: For two days mice received an intraperitoneal (i.p) injection of saline and were placed in an open field chamber to monitor their locomotor activity. On PND37, mice were randomly assigned into treatment groups that received either i.p. methylphenidate (1 or 2mg/kg) or saline, and were again placed in the chambers. On PND38-42, mice received alternating treatment and saline in their home cage. On PND43, mice received treatment and again were placed in the chambers to measure locomotor responses. Aim 2: On PND44, mice were singly housed. From PND47-53, mice received access to 20% EtOH for two hours each day, three hours into their dark cycle. Significant increases in locomotor behavior in response to methylphenidate treatment were observed, regardless of prenatal exposure group. Sensitization to methylphenidate was observed with repeated treatment of 1.0mg/kg. Mice with PAE consumed less alcohol during adolescence than controls, and methylphenidate treatment didn’t affect alcohol consumption. Alcohol exposure early in gestation didn’t significantly affect methylphenidate responses during adolescence. Additionally, PAE impacted subsequent alcohol consumption during adolescence, but not in the expected direction. Future studies should examine alcohol exposure later in development to determine if it may increase subsequent alcohol intake during adolescence.
