Mission

The Herman Lab studies the physiological and behavioral changes associated with alcohol and drug exposure and how neuroadaptations at the circuit, network, and systems level contribute to adverse clinical outcomes including psychiatric disorders like alcohol and substance use disorders, anxiety, and depression.

Research areas

ALCOHOL

Alcohol is one of the most commonly-used substances in the world and while many people drink alcohol, a portion of the population develop pathology in the form of alcohol use disorder (AUD). The Herman lab investigates the effects of acute and chronic alcohol exposure on neuronal activity in brain regions associated with the reinforcing as well as negative affect consequences of alcohol exposure including the central amygdala (CeA), prelimbic prefrontal cortex (PrL PFC) and the brainstem nucleus tractus solitarius (NTS). We are specifically interested in sex differences in the physiological and behavioral consequences of alcohol exposure and how those differences may contribute to differences in vulnerability or AUD risk.

NICOTINE

Nicotine consumption by the use of electronic nicotine delivery systems of vaporized nicotine (or ‘vaping’) is increasing in prevalence in initial users or as an alternative to traditional smoking methods. Our work aims to delineate how nicotine exposure via vapor inhalation affects neuronal activity and synaptic transmission in the mesolimbic reward circuitry, specifically the ventral tegmental area (VTA), the central amygdala (CeA), and the prefrontal cortex, areas that are implicated in the rewarding and reinforcing properties of nicotine as well nicotine aversion and negative affect behavior.

PSYCHEDELICS

Clinical research suggests that psychedelic compounds including psilocybin (or it’s active metabolite psilocin), may have therapeutic potential for treating psychiatric conditions including anxiety, depression, and substance use disorders, however our understanding of the underlying neurobiology of psychedelics is limited. We are investigating the neuroadaptations that occur with psilocybin (or psilocin) administration to uncover information on the neurobiological mechanisms by which psychedelic compounds exert potential therapeutic effects. We are specifically interested in brain region-specific effects of psilocin on corticolimbic circuitry, with a focus on neuronal activity, circuit reactivity/behavioral responding, and brain-wide activity and functional connectivity. We are also investigating the role of  5-HT2A neurons in the actions of psilocin in affective behavior using an integrated electrophysiological, molecular, behavioral, and brain-wide imaging approach.

POLYSUBSTANCE USE

Alcohol and nicotine polysubstance use, particularly involving nicotine vapor, is increasing in prevalence and impact, but the underlying mechanisms of combined use and the contribution to alcohol use disorder (AUD) pathology remain unclear. An improved understanding of the neurobiological mechanisms of alcohol and nicotine vapor co-exposure in mesolimbic circuitry and drinking behavior across stages of co-exposure history would provide important information on the cellular mechanisms underlying behavioral pathology associated with increased risk of AUD as well as potential treatment complications. This information could also aid in identifying vulnerable populations and improving treatment strategies for the negative consequences of alcohol and nicotine co-use.

SOCIAL DOMINANCE BEHAVIOR

Social hierarchy is an evolutionarily-conserved phenomenon with profound influence on health and disease, and atypical social functioning is a common feature of many neuropsychiatric disorders. We are investigating the neural mechanisms underlying social hierarchy and social dominance behavior in both paired and group contexts, and with a special focus on females, where previous studies are limited. We are specifically interested in brain regions implicated in social dominance behavior, including the lateral habenula (LHb) which is involved in processing of social information and as a potential modulator of the valence of social stimuli. Dysregulation of the LHb has been implicated in neuropsychiatric disorders including social anxiety disorder, generalized anxiety, and depression.