Division of Pharmacology and Toxicology
University of Texas at Austin

Research in the Fonken lab at UT Austin broadly focuses on how interactions among the immune, nervous, and endocrine systems regulate complex behavioral processes.

Brain resident immune cells, called microglia, were first identified in the brain by Del Rio-Hortega over 100 years ago. These cells were initially thought to have a passive role in the healthy brain and only become active during CNS injury. We now know that glial cells have a diverse array of functional roles in maintaining brain homeostasis and in responding to CNS pathology. For example, microglia are involved in synaptic development and pruning, neuronal migration, and progenitor cell differentiation.

Microglia function is tightly regulated in the CNS to help regain homeostasis following immune system activation. However, the neuroimmune system is sensitive to a number of environmental challenges and dysregulation of neuroimmune function can occur resulting in a sensitized or “primed” neuroimmune environment. Exaggerated or persistent neuroinflammation due to a primed neuroimmune environment is implicated in neuropsychiatric disorders including depression, schizophrenia, and cognitive dysfunction.

Our current research focuses on understanding how endogenous (e.g. circadian rhythms and aging) and exogenous (e.g. environmental pollutants, infection, and injury) factors can lead to a primed neuroinflammatory environment resulting in cognitive and affective behavioral changes.