I began working on brain derived neurotrophic factor (BDNF) during my Master’s studies. BDNF is a growth factor that during development has been shown to play crucial roles in the development, growth and maintenance of neurons. More recently however, Dr. Lora Kasselman et al., reported that infusion of BDNF into the hippocampus following sympathetic challenge resulted in vascular inflammation. My thesis work focused on replicating the findings and generalizing it to other rat strains and looking at sex as a variable. I was able to replicate Kasselman’s findings and also had an interesting observation of neurodegeneration for some groups but not others, a question that I would like to return to at another time.  In light of the easily replicable results, I decided to move on to another species, namely, mice. Our lab currently has a line of BDNF transgenic mice (genetically altered to overexpress BDNF). Using these mice I now seek to replicate the findings from the rat model. Since these mice are not limited to brain overexpression but also the entire body, I will focus on any potential peripheral organ inflammation which is much more common in human populations. In addition, since this model is based on sympathetic abnormality, I am also interested in determining the potential involvement of neuropeptide Y (NPY). NPY is one of the most abundant and potent neuromodulators and it plays a key role in vasoconstriction which some suggest to be a crucial component of inflammation. Preliminary data (presented at the 2011 society for neuroscience conference) suggests that BDNF plays a key role in peripheral inflammation during sympathetic challenge, a pattern which is dampened by blocking the peripheral NPY receptor 1.  Currently, I am in the process of further elaborating the relationship between BDFN, inflammation and NPY.