Area:
Neuroscience Biology, Behavioral Psychology, Experimental Psychology
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High-probability grants
According to our matching algorithm, Justin Oh-Lee is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2005 |
Oh-Lee, Justin D |
R15Activity Code Description: Supports small-scale research projects at educational institutions that provide baccalaureate or advanced degrees for a significant number of the Nation’s research scientists but that have not been major recipients of NIH support. The goals of the program are to (1) support meritorious research, (2) expose students to research, and (3) strengthen the research environment of the institution. Awards provide limited Direct Costs, plus applicable F&A costs, for periods not to exceed 36 months. This activity code uses multi-year funding authority; however, OER approval is NOT needed prior to an IC using this activity code. |
Cdk-Mediated Striatal Neuroadaptation in Parkinsonism @ Central Michigan University
DESCRIPTION (provided by applicant): Parkinson's disease (PD) is a neurodegenerative disorder currently afflicting nearly over one million Americans. Initially, treatment with levodopa (L-DOPA) or a direct dopamine agonist ordinarily confers substantial clinical benefit. Within a few years, however, repetitive administration of these drugs to PD patients ultimately leads to development of disabling motor response complications. Current evidence suggests that these response alterations involve activation of striatal signal transduction cascades causing upregulation of corticostriatal glutamatergic synaptic transmission which in turn modifies striatal output in ways that compromise motor behavior. FosB-mediated activation of cycline-dependent kinase 5 (Cdk5) has been increasingly implicated in the neuroadaptive mechanisms related to repeated psychostimulant administration in drug addiction. To elucidate molecular mechanisms that underlie the pathogenesis of motor response occurring with chronic L-DOPA treatment of parkinsonian animals, the time course of response shortening and the appearance of Abnormal Involuntary Movements (AIMs) is evaluated in relation to change in striatal Cdk5 and glutamatergic signaling in 6-hydroxydopamine lesioned rats. The striatal tissue from these animals is also evaluated for these biochemical changes by using Western blot, Immunoprecipitation and immunohistochemical analyses. The functional significance of striatal Cdk5 activation is then determined by assessing the ability of Cdk5 antisense and inhibitors to affect both the biochemical and motor response changes associated with chronic dopaminomimetic treatment and its subsequent withdrawal. Findings from the proposed studies can provide more accurate understanding of molecular mechanisms underlying striatal neuroadaptive plasticity contributing to the pathogenesis of LDOPA- induced genesis of maladaptive motor complications in advanced PD, and suggest novel approaches to safer and more effective therapy of extrapyramidal motor dysfunction and other dopamine disease states.
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0.958 |