Neuroscience 2003 Abstract
| Presentation Number: | 948.9 |
|---|---|
| Abstract Title: | Striatal expression change in transferrin is associated with exercise-induced protection against 6-hydroxydopamine. |
| Authors: |
Korade Mirnics, Z.*1
; Mirnics, K.2
; Smith, A. D.3
; Lin, E.3
; Jaumotte, J. D.3
; Douglass, K. C.2
; Macioce, M.2
; Lewis, D. A.2
; Schor, N. F.1
; Zigmond, M. J.3
1Pediatrics, Univ. of Pittsburgh, Pittsburgh, PA 2Psychiatry, Univ. of Pittsburgh, Pittsburgh, PA 3Neurol., Univ. of Pittsburgh, Pittsburgh, PA |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Parkinson's Disease: Models |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Parkinson's Disease: Experimental therapies |
| Session: |
948. Parkinson's Disease: Models VI Poster |
| Presentation Time: | Wednesday, November 12, 2003 1:00 PM-2:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # Y3 |
| Keywords: | MICROARRAY, PARKINSON, NEUROPROTECTION, DOPAMINE |
6-OHDA can be used to selectively destroy dopamine (DA) neurons and thereby produce a model for Parkinson’s disease. When 6-OHDA is administered unilaterally into the medial forebrain bundle, animals show a contralateral sensory and motor neglect that can be used as a measure of the level of degeneration and recovery. Physical exercise leads to complex and well-defined expression changes in the cortex. The forced use of the impaired forelimb after unilateral 6-OHDA lesion protects against gross behavioral impairments and causes a remarkable sparing of striatal DA and VMAT2, a marker of DA terminals (Tillerson et al., 2001). Our recent DNA microarray analysis of sham-lesioned (SH), 6-ODHA lesioned (L) and 6-OHDA lesioned + casted (LC) animals showed a robust upregulation of multiple oligodendrocyte-related transcripts in the striata of LC animals, but not in L animals (Mirnics, SFN, 2002). Transcripts for transferrin (TF), an iron-binding protein secreted in the CNS by oligodenrocytres and ependymal cells, were among the most upregulated gene products. We sought, therefore, to determine if TF was sufficient to protect against oxidative stress in DA neurons. Co-application of TF protein with 6-OHDA (0.5-1 μM) resulted in 20-30% increase in survival of PC12 cells as compared with 6-OHDA alone. This effect was mimicked by the application of TF 24-hr prior to 6-OHDA. The effect of TF was dose-dependent with a most effective protection achieved with 50 μg/kg. Ongoing experiments are examining the effect of TF in other models. These results suggest that exercise produces its protective effects in part by reducing the availability of free iron and thereby reducing oxidative stress on DA neurons.
Supported by RAC CHP (ZKM), NARSAD (KM), Michael J. Fox Foundation (ADS), NS041297 (NFS) and NS19608 (MJZ).
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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