Degenerative Risks for Parkinson's Disease After Toxin Exposure and Stress
Abstract
Parkinson's disease (PD) is caused by deterioration of the dopamine (DA) nigrostriatal system. Loss of DA can be induced experimentally by neurotoxic lesion of DA neurotransmitter producing neurons in the substantia nigra, or through lesioning DA axon terminals in the striatum with subsequent degeneration of their cell bodies in the substantia nigra. We have produced and characterized a new animal model of PD. Experimental PD has been induced by small unilateral, intrastriatal infusions of the neurotoxin 6-hydroxytyramine to produce partial loss of striatal DA. The striata of neurotoxin treated animals were examined morphologically and compared to the unlesioned, contralateral side at two time points following the treatment. Presynaptic striatal DA terminal losses were determined by evaluation of immunohistochemical expression of tyrosine hydroxylase. Differential changes in postsynaptic striatal DA receptor expression occurred at 1 and 4 weeks after neurotoxin exposure. Subsequent experiments examined the effect of exposure to a stressor on further exacerbation of DA receptor changes following the neurotoxin lesion. Neurochemical analysis of residual striatal DA following neurotoxin infusion and stressor exposure was performed in parallel, using HPLC of DA and its metabolites. Some tissue samples are stored and awaiting analysis to be performed over the next few months.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2001
- Accession Number
- ADA400563
Entities
People
- Marjorie A. Ariano
Organizations
- Rosalind Franklin University of Medicine and Science