Dr. Cowan began his interest in nervous system function and development as an undergraduate student at Wesleyan University in the lab of Professor David Adams, PhD. He studied the neuronal basis of aggression in rats using primary behavioral assays and pharmacological manipulation of relevant brain regions. Chris then worked as a research technician for a small biotech company, Sennes Drug Innovations (Houston, TX) where he studied cell cycle arrest induced by the Cdk/Cyclin inhibitor, p21CIP1, a protein induced during cellular senescence and dysregulated in tumor cells.
In 1994, he attended graduate school at Baylor College of Medicine in the lab of Ted Wensel, PhD. In his thesis work, Chris and his colleagues identified and characterized the GTPase activating protein (GAP), RGS9, as an essential regulator of the inactivation phase of the rod photoreceptor light response.
During his postdoctoral training in Michael E. Greenberg’s lab (Harvard Medical School), Chris explored molecular signaling mechanisms that underlie neuronal connectivity during brain development. He focused on two aspects of neuronal connectivity: (1) axon guidance and (2) synapse formation/remodeling. In his studies of axon gudance signaling, Chris identified the actin cytoskeleton regulator, Vav2, as an important signaling component of Eph family axon guidance receptors during axonal targeting in vitro and in vivo. With regards to synapse remodeling, Chris and colleagues found that MEF2 transcription factors regulate synapse number in response to neuronal activity, suggesting a critical negative feedback process to control synaptic connectivity.
Since joining the UTSW faculty in late 2005, the Cowan lab has been studying the role and regulation of MEF2 transcription factors in striatal synaptic and behavioral plasticity during chronic exposure to drugs of abuse. In addition, his lab has been exploring Eph receptor signaling mechanisms involved in retinal and CNS axon guidance during development.
