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.

Effect of Addiction Modeling Reinforcement Schedules on Delay Discounting

Elevated delay discounting, in which delayed rewards quickly lose value as a function of time, is associated with substance use and abuse. Currently, the direction of causation is unclear: while some research indicates that elevated delay discounting leads to future substance use, it is also possible that chronic substance use and specifically the rate of reinforcement associated with drug use, leads to elevated delay discounting. This project aims to examine the latter possibility. 47 participants completed ten 30-minute daily sessions of a visual attention task, and were reinforced at a rate intended to model drug use (fixed ratio 1) or drug abstinence (fixed ratio 10). Baseline and post-training rates of delay discounting were assessed for hypothetical $50 and $1000. Area under the curve of the indifference points as a function of delay was calculated. A greater area under the curve suggests more self-control, whereas a lower value represents more impulsiveness. Results at the monetary value of both $50 and $1000 showed increased impulsivity in relation to the control for both the FR1 and FR10 groups indicating that the two schedules may both model drug use.

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.