Mission & Goals
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
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.
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