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.

Executive functions like attention rely on well-conserved brain circuitries to allow us to navigate through our complex environment. Many neurodegenerative and neuropsychiatric disorders involve a deficit in the ability to detect and use these environmental cues to guide ongoing behavior. We hypothesize that these deficits may result from dysfunction of the connection between the mediodorsal thalamus (MD) and the regions of the prefrontal cortex (prelimbic PFC (PRL) and anterior cingulate cortex (ACC), but the unique contributions of the MD’s relay to each of these subregions in the context of cue-guided behavior has yet to be uncovered. My dissertation therefore focuses on 1) better understanding the structure of the mediodorsal thalamus, 2) categorizing the information processed by the MD itself and the information received by the MD’s terminal fields in the cortex (PRL and ACC), and 3) assessing necessity of each of these important cognitive regions to cue detection. Using wild type mice, I measure these regional changes in brain activity in both classical and instrumental conditioning by utilizing in vivo calcium imaging and analyzing changes around task events, such as a light cue that predicts the delivery of a reward.