The Effect of Dietary Tartrazine on Brain Dopamine and the Behavioral Symptoms of Attention Deficit Hyperactivity Disorder

Attention Deficit Hyperactivity Disorder is a neurodevelopmental disorder correlated with a decrease in brain dopamine and an increase in behavioral symptoms of hyperactivity and impulsivity. This experiment explored how tartrazine (Yellow #5) impacts these symptoms. After tartrazine administration to Spontaneously Hypertensive Rats (SHR), dopamine concentrations in regions of brain tissue were measured using Enzyme-Linked Immunosorbent Assay analysis. Behavioral testing with a T-maze and open field test measured impulsivity and hyperactivity, respectively. Results indicate that dietary tartrazine increases hyperactive behaviors in the SHR. However, results do not indicate a relationship between dietary tartrazine and brain dopamine. No conclusions regarding the relationship between dietary tartrazine and impulsivity were drawn.

The relationship of early social, mental, and behavioral experiences with adult obesity and Alcohol Use Disorder

Stressful life events early in life, including symptoms of mental disorders or childhood maltreatment, may increase risk for worse mental and physical health outcomes in adulthood. The purpose of this dissertation was to examine the effects of childhood Attention Deficit Hyperactivity Disorder (ADHD) symptoms and maltreatment experience on two adult outcomes: obesity and alcohol use disorder (AUD). Mediational effects of adolescent characteristics were explored. This dissertation used Waves I, III, and IV of the National Longitudinal Study of Adolescent to Adult Health. In Paper 1 (Chapter 3), we investigated the association between multiple types of child maltreatment and adult objective (body mass index; BMI) and subjective (self-rated) obesity, as well as mediating effects by adolescent characteristics including depressive symptoms and BMI. Results showed that after adjusting for sex, race/ethnicity, and maternal education, physical maltreatment was moderately associated with adulthood obesity as measured by BMI and self-reported obesity, while sexual maltreatment was more strongly associated with the objective measure but not the subjective measure. The indirect effects of mediation of adolescent BMI and depressive symptoms were statistically significant. In Paper 2 (Chapter 4), the objective was to examine mediation by adolescent depressive symptoms, alcohol consumption, peer alcohol consumption, and delinquency in the relationship between ADHD symptoms and adult AUD. The indirect effects of mediation of adolescent delinquency, alcohol consumption, and peer alcohol consumption were statistically significant in single and multiple mediator models. In Paper 3 (Chapter 5), the objective was to assess the joint effects of maltreatment/neglect on adult AUD. After adjusting for sex, race/ethnicity, child maltreatment, and parental AUD, ADHD symptoms were significantly associated with increased odds of AUD. There was no strong evidence of multiplicative interaction by maltreatment. This association was stronger for males than females, although the interaction term was not statistically significant. This dissertation adds to the literature by examining relationships between several major public health problems: ADHD symptoms, childhood maltreatment, AUD, depressive symptoms, and obesity. This project has implications for understanding how early life stress increases risk for later physical and mental health problems, and identifying potential intervention targets for adolescents.

The Impact of Prenatal Nicotine Exposure on Impulsivity and Neural Firing in the Medial Prefrontal Cortex

Prenatal nicotine exposure (PNE) is linked to a large number of psychiatric disorders, including attention deficit hyperactivity disorder (ADHD). Current literature suggests that core deficits observed in ADHD reflect abnormal inhibitory control governed by the prefrontal cortex (PFC) of the brain. The PFC is structurally altered by PNE, but it is still unclear how neural firing is affected during tasks that test behavioral inhibition, such as the stop-signal task, or if neural correlates related to inhibitory control are affected after PNE in awake behaving animals. To address these questions, we recorded from single medial PFC (mPFC) neurons in control rats and PNE rats as they performed our stopsignal task. We found that PNE rats were faster for all trial types and were less likely to inhibit the behavioral response on STOP trials. Neurons in mPFC fired more strongly on STOP trials and were correlated with accuracy and reaction time. Although the number of neurons exhibiting significant modulation during task performance did not differ between groups, overall activity in PNE was reduced. We conclude that PNE makes rats impulsive and reduces firing in mPFC neurons that carry signals related to response inhibition.