Bioanalytical Research Laboratory

The Bioanalytical Research Laboratory is an interdisciplinary resource for all LECOM researchers. The Instrumentation includes High Performance Liquid Chromatography (HPLC) with electrochemical detection. Currently the HPLC system is configured to determine the concentration of the neurotransmitters dopamine and serotonin and their metabolites in either tissue or serum samples.

The BRL’s 3-D Microscopy center is resource for all LECOM researchers. The center currently includes an Edge R400 stereomicroscope, which produces high power (up to 100x objectives) images in real time using multiple oblique white light illumination. The stereo image can be produced by using either a red-green or red-blue anaglyph lighting, or the use of polarize light. The photo to the left is a red-green anaglyph and can be viewed using the red-green glasses (left eye red / right eye green. We are currently in the process of acquiring an inverted microscope and will retrofit this microscope with the multiple oblique technology.

My current research interests focus mostly on Parkinson disease and Schizophrenia. I also have a personal interest in Autism. My primary project is a collaborative project that studies the effects of a mouse model with an altered FGFR1 gene. Previous literature indicated a possible involvement of defective signaling at this receptor and the progression of Parkinson Disease. This alteration, studied here, negatively affects the tyrosine kinase domain of this receptor protein. Along with my collaborator, we have shown significant alterations in the dopamine levels in the striatum region of the brain, as measured by HPLC analysis. Our initial studies indicated that we had a possible model for Parkinson Disease. (Molecular Brain Research 139 (2005) 361–366 – “Transfection of tyrosine kinase deleted FGF receptor-1 into rat brain substantia nigra reduces the number of tyrosine hydroxylase expressing neurons and decreases concentration levels of striatal dopamine.”) However, a following study done in a genetically alerted mouse line gave us data that looked more like schizophrenia, in other words, dopamine levels were increased. (Journal of Neurochemistry 97 (2006) 1243-1258 – Fibroblast growth factor receptor signaling affects development and function of dopamine neurons – inhibition results in a schizophrenia-like syndrome in transgenic mice.) The behavior of these mice normalize when given anti-schizophrenic medication. The logical follow up was to look at the serotonin system. (Schizophrenia Research 113 (2009) 308-21 – Serotonergic hyperinnervation and effective serotonin blockade in an FGF receptor developmental model of psychosis.) We found an increase of serotonin and very interestingly, these mice normalized their behavior following treatment with atypical anti-schizophrenic medication. Current ongoing studies show that these mice may be more vulnerable to dopaminergic toxins thus they may still have be useful as a Parkinson Disease model. I anticipate continuing this collaboration with the people in Buffalo. My personal research that overlaps this collaboration involves dopamine metabolites, specifically DOPAL. This is the aldehyde oxidation product of dopamine.

I am also interested in Autism because I am the father of an Autistic child, however, I don’t have any studies in this area yet. So my future plans are to continue my collaborations in the FGFR1 (TK-) field, performing much of the HPLC and some of the histology and to further pursue the dopamine metabolite toxicity field.