Core B: Goals Al. In order to provide consistency and the highest quality of catecholamine quantitation, Core B will provide all sub-projects with well-controlled analytical chemistry services via high performance liquid chromatography with electrochemical detection (HPLC-EC) employing state-of-the-art coulometric array detection. A2. Core B will provide relative gene-expression quantitation via Real Time RT-PCR using both low density arrays, as well as quanititation of individual genes as directed by sub-project investigators. In addition, Core B will also be a resource to troubleshoot develop and run ELISAs and/or western blots to determine whether key changes in gene expression result in concomitant changes in protein expression as needed. A3. Core B will provide both single- and double-labeling in situ hybridization and analyses of both film and emulsion autoradiography. This will afford determination of both regional localization and semi-quantitative analysis of mRNA expression as well as cellular resolution for determination of cellular phenotype. A4. Finally, surgical services from all of the projects have been moved into Core B. This will allow Core B to provide surgical services for the 6-OHDA lesion studies associated with all of the subprojects. Funneling subjects of all projects through Core B to provide consistent surgical services will further enhance the Center's ability to provide cross project quality control.

Public Health Relevance

The purpose of this core application is to provide support services for a large center focused on examining problems and potential therapeutic solutions for Parkinson's disease. The core will conduct animal surgeries, quantify molecules from tissues of those animals, analyze the results of such experiments and communicate those results back to the project leaders.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS058830-04
Application #
8382685
Study Section
National Institute of Neurological Disorders and Stroke Initial Review Group (NSD)
Project Start
Project End
Budget Start
2012-08-01
Budget End
2013-07-31
Support Year
4
Fiscal Year
2012
Total Cost
$282,078
Indirect Cost
$102,410
Name
Michigan State University
Department
Type
DUNS #
193247145
City
East Lansing
State
MI
Country
United States
Zip Code
48824
Fischer, D Luke; Manfredsson, Fredric P; Kemp, Christopher J et al. (2017) Subthalamic Nucleus Deep Brain Stimulation Does Not Modify the Functional Deficits or Axonopathy Induced by Nigrostriatal ?-Synuclein Overexpression. Sci Rep 7:16356
Fischer, D Luke; Kemp, Christopher J; Cole-Strauss, Allyson et al. (2017) Subthalamic Nucleus Deep Brain Stimulation Employs trkB Signaling for Neuroprotection and Functional Restoration. J Neurosci 37:6786-6796
Collier, Timothy J; Srivastava, Kinshuk R; Justman, Craig et al. (2017) Nortriptyline inhibits aggregation and neurotoxicity of alpha-synuclein by enhancing reconfiguration of the monomeric form. Neurobiol Dis 106:191-204
Kneynsberg, Andrew; Collier, Timothy J; Manfredsson, Fredric P et al. (2016) Quantitative and semi-quantitative measurements of axonal degeneration in tissue and primary neuron cultures. J Neurosci Methods 266:32-41
Polinski, Nicole K; Manfredsson, Fredric P; Benskey, Matthew J et al. (2016) Impact of age and vector construct on striatal and nigral transgene expression. Mol Ther Methods Clin Dev 3:16082
Madhavan, Lalitha; Daley, Brian F; Davidson, Beverly L et al. (2015) Sonic Hedgehog Controls the Phenotypic Fate and Therapeutic Efficacy of Grafted Neural Precursor Cells in a Model of Nigrostriatal Neurodegeneration. PLoS One 10:e0137136
Grabinski, Tessa M; Kneynsberg, Andrew; Manfredsson, Fredric P et al. (2015) A method for combining RNAscope in situ hybridization with immunohistochemistry in thick free-floating brain sections and primary neuronal cultures. PLoS One 10:e0120120
Paumier, Katrina L; Luk, Kelvin C; Manfredsson, Fredric P et al. (2015) Intrastriatal injection of pre-formed mouse ?-synuclein fibrils into rats triggers ?-synuclein pathology and bilateral nigrostriatal degeneration. Neurobiol Dis 82:185-199
Polinski, Nicole K; Gombash, Sara E; Manfredsson, Fredric P et al. (2015) Recombinant adenoassociated virus 2/5-mediated gene transfer is reduced in the aged rat midbrain. Neurobiol Aging 36:1110-20
Fischer, D Luke; Collier, Timothy J; Cole-Strauss, Allyson et al. (2015) High-Frequency Stimulation of the Rat Entopeduncular Nucleus Does Not Provide Functional or Morphological Neuroprotection from 6-Hydroxydopamine. PLoS One 10:e0133957

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