Kaufer Laboratory

Research in the Kaufer lab focuses on understanding how stress affects the brain. While we are primarily a molecular neuroscience lab, we use interdisciplinary approaches ranging from cell culture to behavioral analysis, and frequently collaborate to expand our methods of analysis. Under the umbrella of stress research, we have a diverse array of past and current projects.


Current Projects Include:

Epilepsy Graphic

Long-Term Consequences of Early Life Stress:

Our preliminary data has shown that stress increases the production of oligodendrocytes in the brain – a cell type that produces the myelin sheaths that wrap the axons of neurons, thereby regulating the propagation of neural impulses. We hypothesize that early life stress, especially during the critical period of myelination that happens after birth, may alter the extent of myelination in the brain, leading to structural hypermyelination that persists into adulthood. We are investigating this as a model for how early life stress may create vulnerability for mental illnesses that manifest later in life, such as post-traumatic stress disorder and depression. In collaboration with Prof. Darlene Francis in the Department of Public Health, were a using natural variations in rat grooming behavior to characterize differences in myelination throughout life in rats that were reared in high grooming or low grooming environments. We are also initiating projects to expand these findings to humans by performing MRI imaging of myelination in human populations that have experienced early life stress.


Epilepsy Research:

In collaboration with the laboratory of Alon Friedman (Ben-Gurion University, Israel), we are studying the mechanisms of epileptogenesis that follow traumatic brain injury and precede the onset of clinical epilepsy. We hypothesize that disruption of the blood-brain barrier (BBB), as occurs after head injury, is a major precipitating event in triggering epileptogenesis. Using rodent models, we have shown that albumin, a major component of the blood, enters the brain during BBB dysfunction.  Once in the neuropil, albumin is able to bind to TGF-β receptors and activate the TGF-β signaling pathway, triggering a regulatory cascade that modulates inflammation and neuroexcitability. Critically, we have shown that blocking albumin from binding to and activating the TGF-β receptor prevents subsequent epileptiform activity and onset of spontaneous seizures. We are currently investigating the mechanistic details by which TGF-β signaling contributes to epileptogenesis, as well as translating our findings towards the clinical context by investigating the efficacy of drugs that block the TGF-β receptor.


The Role of Hippocampal Stem Cells in Emotional Memory:

Emotional context provides a means to regulate the strength of memory, for instance differentiating a fearful memory from those of routine, daily events. The emotional timbre of memory is encoded in part by connections between the amygdala and hippocampus. While new neurons generated from a unique population of stem cells in the hippocampus have been shown to be important for memory generally, our research has shown that they may have roles specifically in regulating emotional affect. Using the rat model, we have shown that disrupting input from the amygdala to the hippocampus not only decreases the rate of hippocampal neurogenesis, but also suppresses the activation of these new neurons in response to fear input. We are currently investigating the molecular mechanisms that underlie amygdala influence over the production and function of new neurons in the hippocampus, which offers intriguing insights into the role of these new neurons in regulating the plasticity of the emotional aspect of memory.