Research 

Anxiety and mood disorders are the most common emotional disorders in adolescents, with suicidal ideation affecting up to 50% of youth. Adolescence is a remarkable period of neuroplasticity in the amygdala, a well-conserved structure best known for its role in emotional behaviors. Although in many cases adaptive, the capacity for neural circuit alteration also induces a state of vulnerability to environmental perturbations.

In modern societies, adolescents are increasingly subjected to irregular environmental lighting, as 80% of adolescents in the USA reported using computers, smartphones, and tablets at night-time. Altered environmental light is associated with increased risk of psychiatric disorders. An important sub-nucleus of the amygdala, the medial amygdala (MeA) is situated in a crucial position to link environmental lighting to brain regions regulating emotional responses. 

Using a translational mouse model, this project explores the effects of alerted patterns of light exposure on amygdala plasticity and emotion-related behavior in adolescent mice, which will potentially lead to new complementary strategies to advance health and well-being in human adolescents.

This project is funded by NIH-NCCIH (K99/R00-AT010903)

Depression is one of the most common, disabling, and expensive of all neuropsychiatric disorders. Emerging evidence implicates circadian rhythm abnormalities in the pathophysiology of depression. In particular, the nucleus accumbens (NAc), a central component of the midbrain dopamine reward circuit, exhibits disturbed circadian rhythms in postmortem brains of depressed patients, as well as in stressed mice exhibiting helpless behavior. 

We previously found that higher levels of the core circadian clock protein CRYPTOCHROME in the NAc may block D1 dopamine receptor activation during the nocturnal active phase of mice, thereby compromising normal daily activation of NAc neurons and leading to helpless behavior. 

This project studies the role of the circadian gene CRYPTOCRHOME in regulating neuronal physiology in the NAc to increase antidepressant efficacy through time dosing administration (chronopharmacology). 

This project is funded by NIH-NIMH (R21MH1352O7)

Light profoundly influences human health by rewiring the central circadian clock. These circadian responses to light orchestrate the synchronization of behavior and physiology, ensuring they align with the daily and seasonal shifts in the environment. In mammals, circadian and seasonal responses to light require the suprachiasmatic nucleus (SCN), which is the central daily clock and annual calendar regulating physiology and behaviors. Alterations in light/dark cycles and circadian rhythms have been associated with an increased incidence of certain health conditions, including cancers, metabolic dysfunctions, infertility, and psychiatric disorders. 

We recently found a previously unknown molecular adaptation in the SCN involving changes in neurotransmitter phenotype in response to photoperiod. This is a newly recognized form of neuroplasticity that involves the loss of one neurotransmitter and the gain of another in the same neuron, effectively changing the phenotype and function of the cell. Despite recent progress, our understanding of photoperiodic plasticity in the circadian pacemaker is far from complete. 

This project aims at characterizing the molecular and cellular mechanisms underlying photoperiodic neurotrasmitter plasticity in the SCN network.