Date of Award

5-2021

Document Type

Thesis

Degree Name

Master of Arts in Psychological Science

Department

Psychology

First Reader/Committee Chair

Cynthia Crawford

Abstract

Attention deficit hyperactivity disorder (ADHD) is a common developmental disorder characterized by impulsivity, inattention, and hyperactivity. In rodents, neonatal 6-OHDA lesions is an established model of ADHD because it produces symptoms of hyperactivity and cognitive deficits that improve following psychostimulant treatment. Recently, early alcohol exposure in rodents has also been suggested as a model of ADHD due to the high prevalence of ADHD in children exposed prenatally to alcohol. However, children exposed to prenatal alcohol differ in symptoms from children with idiopathic ADHD, suggesting that ADHD caused by prenatal alcohol exposure may be a special subtype of ADHD or a completely different disorder. The aim of the present study was to compare the 6-OHDA lesion model with the effects of early alcohol exposure on hyperactivity, psychostimulant response, and passive avoidance learning in preweanling rats. It was hypothesized that alcohol exposure and the combined effects of a 6-OHDA lesion and exposure to alcohol would result in increased locomotor hyperactivity and poorer performance on the passive avoidance task. A total of 1,053 male and female Sprague-Dawley rats were lesioned with 6-OHDA or placed in a lesion control group on postnatal day (PD 3). Beginning on PD 4, rats were exposed to alcohol (0, 0.3, or 3 g/kg) for six consecutive days or were unhandled. On PD 19, rats were habituated to a locomotor chamber for 60 min. On the following day (PD 20), the rats were injected with amphetamine (1 mg/kg), methylphenidate (2.5 mg/kg) or saline and locomotor activity was measured for 60 min. On PD 23, a separate group of rats were trained on a passive avoidance task and retention was tested for three consecutive days. Our results demonstrated that exposure to a low dose of alcohol can cause an increase in the locomotor activity of female rats, while exposure to a high dose of alcohol can disrupt memory. In addition, our results indicated that 6-OHDA lesions and alcohol exposure do not have an additive effect. In summary, these data suggest neonatal alcohol can cause a dose dependent increase in ADHD-like symptoms.

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