Our Research

The midbrain-forebrain dopaminergic circuitries partake in several important processes, one of which is survival-essential ingestion. We ask how macronutrients, alone or together, signal the brain from the gut to repeat this behavior. Which specific circuits are rallied—and reinforced—by which particular post-ingestive signals, bypassing all ordinarily perceived visual, olfactory, and initial gustatory cues? Is there a causal role by post-ingestive signals in inducing reward learning? Our research has the potential to shed light on dysfunctional reward-related eating in depression, addiction, and obesity. To these ends, we leverage genetic mouse lines (e.g., TRAP2 and DAT-Cre), cell-specific biosensors (ChR2, dLight1.1), optogenetic stimulation, and photometric recoding in our multimodal experimentation.

Acute and chronic stressors can robustly affect food preference, shifting it towards food items that may exacerbate cardio-metabolic risk associated with psychiatric illness. The neural mechanisms behind this relationship are unclear. Recent studies have shown that the nutritional profile of food also has a major influence on how the brain encodes its reward value. Specifically, peripherally-generated, post-ingestive signals of both fat and carbohydrate modulate midbrain dopamine (DA) systems via discrete pathways. My on-going experiments are exploring the mechanisms underlying these sex-specific effects of stress on meso-striatal DA encoding of food reward using multi-region photometry and fluorescent DA reporters.

Alec's research interrogates how the peripheral digestive system is linked to brain reward circuitry and what the connection is between neural activity at the time food is being consumed and signals that are relayed from the gut to the brain after the food has been digested. More specifically, we are looking at how different types of food (ie. fats vs carbohydrates) affect midbrain dopamine during consumption versus post-ingestion to modulate behavior.

Circuits in the thalamus have been heavily studied in the context of neurons, but there is a significant gap in knowledge regarding astrocytic thalamic inputs. Along with astrocytes, I am interested in how neuromodulators such as norepinephrine and dopamine impact circuitry in areas such as the mediodorsal thalamus, the thalamic reticular nucleus, and the prefrontal cortex. To study this, I use viral and fiber implants within the brain, DREADDs, and behavioral techniques to determine the inner workings of these circuits.

Many neurodegenerative and neuropsychiatric disorders involve a deficit in the ability to use environmental cues to guide ongoing behavior. We hypothesize that these deficits may result from dysfunction of the thalamic reticular nucleus (TRN), often considered the brain's "attentional searchlight". This region receives inputs from all major neuromodulator systems (5HT, DA, NE, and ACh), but the unique contributions of each one in the context of cue detection have yet to be uncovered. My dissertation therefore focuses on how each system contributes to TRN control of the MD-PFC cue detection circuit. Using transgenic mouse lines and viral tracing techniques, we are working to determine the anatomy of these neuromodulator inputs to the TRN. To understand how each of these guides behavior, we are utilizing different learning paradigms to measure baseline abilities in attending to and responding to stimulus cues. In vivo calcium imaging will be used to identify the underlying biological mechanisms of these behaviors, and future studies will use DREADDs to selectively manipulate each ascending system to gain an understanding on how each uniquely modulates circuit activity and behavior.