Attention-deficit hyperactivity disorder (ADHD) may be caused by genetic or environmental factors. Among environmental factors, perinatal complications are related, such as neonatal hypoxia-ischemia (HI). Thus, the aim of this study was to investigate whether HI contributes to the development of characteristics related to ADHD in adult rats, and to correlate the behavioral results with brain damage volume. Male Wistar rats were divided into 2 groups: HI and control. The HI procedure consisted of a permanent occlusion of the right common carotid artery followed by a period of hypoxia (90 min; 8% O₂ and 92% N₂) on the 7th postnatal day. Two months later, animals were evaluated in the open field test during a single 5-min session, and in the 5-choice serial reaction time task (5-CSRTT), over 25 weeks. Our results demonstrated that animals submitted to HI manifest cognitive impairments in task acquisition, deficits in sustained attention, and increases in impulsivity and compulsivity in response to task manipulation in the 5-CSRTT. Locomotor activity observed in open field did not differ between groups. Moreover, brain volume loss in the total hemisphere, cerebral cortex, white matter, hippocampus, and striatum were observed in HI animals, especially on the side ipsilateral to the lesion. From these results, we can infer that neonatal HI is an environmental factor that could contribute to the development of behavioral characteristics observed in ADHD that are associated with general brain atrophy.

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Adolescence is an important neurodevelopmental stage for brain sites that are related to the impulse control and reward systems. Alcohol abuse during this period may cause irreversible modifications of neural circuits that are linked to impulsivity. The present study evaluated the effects of alcohol ingestion during adolescence in Wistar rats on anxiety, risk-taking, and impulsive behavior parameters during adulthood. Male Wistar rats (n ϭ 40) were randomly assigned to 1 of 3 treatments: 0, 1, and 3 g/kg alcohol administered orally over 9 sessions, from postnatal Day 31 to 50. Anxiety and risk-taking behaviors were assessed in the elevated plus maze soon after adolescence and during adulthood, and impulsivity was assessed in the operant delay-discounting task in adulthood. None of the alcohol treatments altered risk-taking or impulsive behavior compared with the control group. The group that received 3 g/kg alcohol exhibited less anxiety-like behavior in the first exposure to the elevated plus maze compared with the control group. The results are discussed with regard to the doseresponse, frequency, duration, and age of exposure and route of administration.