Abstract on my Summer research at Michigan State University's Neuroscience department

1. RESEARCH TITLE: PARKIN AS A POTENTIAL NEUROPROTECTIVE AGENT
IN A MOUSE MODEL OF PARKINSON’S DISEASE
FACULTY NAME: Keith J. Lookingland, PhD
DEPARTMENT: Pharmacology and Toxicology
STUDENT NAME: Veronica R. Ortiz
ABSTRACT:
Parkinson’s disease (PD) is a disorder that causes degeneration of midbrain
nigrostriatal dopamine (NSDA), but spares tuberoinfundibular dopamine (TIDA)
neurons (Behrouz B., et al. 2006). MPTP (1-methyl-4-phenyl-1,2,3,6-
tetrahydropyridine), a complex I inhibitor, is used to model PD in mice. Preliminary
studies from have demonstrated that TIDA neurons are resistant to MPTP
neurotoxicity. Furthermore, this resistance is correlated with an increase of parkin
mRNA (Behrouz B., et al. 2006. Neuroscience. 147:592-598). The purpose of the
current study is to determine if MPTP’s effect on DA concentrations in TIDA
neurons and NSDA neurons is correlated with changes in parkin protein expression.
A dose response and a time course analysis of MPTP administration clearly
demonstrated that MPTP causes dose and time dependent loss of DA in the striatum
as well as a transient increase followed by a decrease of parkin protein in the SN. It
was also found that MPTP causes dose and time dependent increase in parkin protein
in the Mediobasal Hypothalamus. This data is consistent with the hypothesis that
parkin may be part of the mechanism responsible for MPTP resistance in TIDA
neurons.