My research examines the cellular and molecular mechanisms underlying sex-specific behaviors and how perturbations during adolescent development disrupt the emergence and maintenance of such behaviors. In many species, sex differences in behavior are necessary for the perpetuation of the species and disruptions of such behaviors during adolescent development can have profound effects on sex-specific behaviors associated with natural reward and motivation (e.g. copulation, aggression, social interaction). In humans, the adolescent period is associated with the emergence of psychiatric disorders involved in motivation and reward including mood and substance use disorders, both of which display substantial sex differences in their prevalence and presentation. We use a range of cellular and molecular approaches to understand how sex differences in adolescent brain development are shaped by environmental experiences. Our hope is that by understanding how the brain develops during adolescence, how environmental factors influence adolescent development and how these experiences result in long-term alterations in behavior, our research will identify sensitive windows for intervention and develop novel therapeutics for all vulnerable populations.
Characterize functional mechanisms of sex-specific circuitry in reward and motivation
Previous studies have indicated sex differences in susceptibility to psychiatric disorders in humans and related behaviors in rodents. Others have identified sex differences in circuitry within the rodent brain, suggesting that underlying sex differences within the brain’s circuitry may regulate sex differences in behavior. Therefore, one goal or our current research is to evaluate functional sex differences in circuitry within the rodent brain. Using retrograde tracing techniques coupled with projection specific chemogenic manipulations we hope to identify how sex differences in circuitry manifest as sex differences in behavior and vulnerability to affective and substance use disorders
Development of Sex-Specific Behavioral Models of Psychiatric Disorders
Even though there are vast sex differences in the presentation and prevalence of psychiatric disorders in humans, most translational models of psychiatric disorders have been development and validated in males. One goal of our research is to not only validate common behavioral models of psychiatric disorders in females but also determine how and why these behavioral strategies differ between the sexes. As a postdoc, I showed that adolescent stress disrupts sex differences in anxiety-related behaviors and alters sex differences in cocaine related behaviors. By using a disrupted model of sex-specific behavior coupled with more advanced computational analysis we hope to understand which aspects of ethologically relevant sex-specific behavioral approaches manifest as differences in susceptibly and resilience to translational models of psychiatric disorders including affective and substance use disorders.
Understand the Cellular and Molecular Mechanisms Underlying Sex-Specific Behaviors
Sexual differentiation of the brain and behavior has been studied as an example of experience-dependent programming for decades. Traditionally, the perinatal period in rodents has been considered the critical window of sexual differentiation of the brain and was considered to be a permanent and inflexible program that could not be disrupted once the window was closed. In recent years, the adolescent period has been hypothesized to be another critical window for sex-specific behavioral programming. My previous research has shown that sex-specific behavior in adulthood can be disrupted specifically by adolescent social stress. Many of the behaviors investigated are related to motivation and reward and serve as translational models of affective and substance use disorders. An overall goal of the lab is to determine how these sex-specific behavioral outcomes are programmed during adolescence at the transcriptomic, epigenomic and proteomic level. Using a disrupted model of sex-specific behaviors we can develop testable hypotheses of the molecules and cellular mechanisms critical for the developmental programming of such behaviors. Through this, we hope to identify developmental windows for therapeutic interventions for vulnerable populations.