Research Projects
Prenatal Alcohol and Brain Circuits
Fetal Alcohol Spectrum Disorder (FASD) is the most common preventable cause of mental retardation. While the reasons why a mother chooses to drink varies from person to person, the impact it has on the developing fetus can range from full blown Fetal Alcohol Syndrome (FAS) to mild neurobehavioral deficits. Individuals with FASD often suffer from deficits in emotion processing, such as anxiety, which may contribute to a number of problems, including drug abuse and alcoholism, and can have profound effects from infancy to adulthood. Using models of prenatal alcohol exposure, we are interested in examining adaptations in modulatory neurotransmitter systems, such as dynorphin/kappa opioid receptor and corticotropin-releasing factor, within various neural circuits that result from prenatal alcohol exposure that may contribute to deficits in emotion processing.
Prenatal Opiate Exposure
The recent opioid epidemic has resulted in a multitude of issues worldwide, including increased use of opiates during pregnancy and neonatal opioid withdrawal syndrome (NOWS). While studies have focused on understanding and treating NOWS, little is known about the long-term consequences of prenatal opioid exposure in the offspring. Human and animal studies have indicated that the most commonly reported deficits in offspring exposed to opiates in utero include alterations in emotion processing (i.e. anxiety and stress-reactivity) and impaired learning, memory, and cognitive function. However, the mechanisms and/or neuroadaptations underlying these behavioral alterations remain unknown. Using a animal model, we are studying the long-term effects of prenatal methadone exposure, an FDA approved medication-assisted opioid therapy for pregnant women with an opioid use disorder, on structures involved in cognitive function and emotion processing, including the hippocampus and amygdala.
Autism and Alcohol Use
Austism spectrum disorder (ASD) is among the most common neurodevelopmental disorders, characterized by 3 typical neurobehavioral symptoms (alterations in social behaviors, repetitive and/or restricted movements, and deficits in language). Surprisingly, the prevalence of alcohol and substance misuse is shockingly high in individuals with ASD, with estimates that people with ASD are twice as likely to develop an alcohol or substance use disorder. Despite these statistics, the neurobiological mechanisms underlying the relationship between ASD and increased risk for alcohol misuse is completely unknown. Using the valproic acid animal model of ASD, we have begun to explore potential neural substrates that may link ASD and alcohol misuse.
