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BackgroundPrenatal ethanol exposure (PE) causes multiple behavioral and cognitive deficits, collectively referred to as fetal alcohol spectrum disorders (FASD). Studies show that 49–94% of FASD children exhibit attention deficits, even when they have normal IQs or lack severe facial deformities, suggesting that attention deficits could be caused by even moderate prenatal exposure to alcohol, of which the underlying neural mechanisms are still unclear. A valid rodent model could help elucidate this phenomenon.Materials and MethodsA second-trimester equivalent binge drinking PE model was utilized. Pregnant Sprague Dawley rats were administered with 15% (w/v) ethanol (6 g/kg/day, via gastric gavage) during gestational days 8–20, and their offspring were the subjects in the present study. A modified 2-choice reaction time (2-CRT) task was used to illustrate possible attention deficits, including increased action impulsivity and lapses of attention. Enhanced impulsivity was reflected by more premature responses while increased lapses of attention were manifested as more incorrect responses and/or greater variability of reaction time, demonstrated by more skewed distributions of reaction time. Ten-week-old male and female rats were tested for three sessions following 16–19 days of training.ResultsOur PE paradigm caused no major teratogenic effects. PE led to increased impulsivity exhibited as greater premature responses and augmented lapses of attention shown by greater skewnesses of reaction time distributions, relative to controls. The deficits were observed in both PE male and female rats. Interestingly, in males, the attention deficits were detected only when the 2-CRT task was relatively difficult whereas in females they were detected even when the task was at a less demanding level.ConclusionWe show that the binge drinking pattern of PE led to attention deficits in both sexes of rats even though no major teratogenic effects were observed. Therefore, this rodent model can be used to study neural mechanisms underlying attention deficits caused by PE and to explore effective intervention approaches for FASD.

In this paper we propose an integrative model of habituation of reinforcer effectiveness (HRE) that links behavioral and neural based explanations of reinforcement. We argue that habituation of reinforcer effectiveness (HRE) is a fundamental property of reinforcing stimuli. Most reinforcement models implicitly suggest that the effectiveness of a reinforcer is stable across repeated presentations. In contrast, an HRE approach predicts decreased effectiveness due to repeated presentation. We argue that repeated presentation of reinforcing stimuli decreases their effectiveness and that these decreases are described by the behavioral characteristics of habituation (McSweeney and Murphy, 2009;Rankin et al., 2009). We describe a neural model that postulates a positive association between dopamine neurotransmission and HRE. We present evidence that stimulant drugs, which artificially increase dopamine neurotransmission, disrupt (slow) normally occurring HRE and also provide evidence that stimulant drugs have differential effects on operant responding maintained by reinforcers with rapid vs. slow HRE rates. We hypothesize that abnormal HRE due to genetic and/or environmental factors may underlie some behavioral disorders. For example, recent research indicates that slow-HRE is predictive of obesity. In contrast ADHD may reflect ‘accelerated-HRE’. Consideration of HRE is important for the development of effective reinforcement based treatments. Finally, we point out that most of the reinforcing stimuli that regulate daily behavior are non-consumable environmental/social reinforcers which have rapid-HRE. The almost exclusive use of consumable reinforcers with slow-HRE in pre-clinical studies with animals may have caused the importance of HRE to be overlooked. Further study of reinforcing stimuli with rapid-HRE is needed in order to understand how habituation and reinforcement interact and regulate behavior.