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Effect of MPTP on dopaminergic neurons in the goldfish brain: a light and electron microscope study
G Goping1, H B Pollard, O M Adeyemo
1Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Abstract:
The neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) causes a Parkinsonian syndrome in the goldfish (Carassius auratus), characterized by transient bradykinesia, the accumulation of MPP+ in the brain, and a decrease in the forebrain and midbrain content of catecholamines (Pollard et al., FASEB J., 6 (1992) 3108-3116). Using light and electron microscopy, we studied the effect of MPTP on the distribution and ultrastructure of tyrosine hydroxylase (TH)-immunoreactive, dopaminergic neurons, and on the ultrastructure of other selected areas of the goldfish brain. Goldfish were treated with MPTP (50 mg/kg) in the absence or presence of L-deprenyl (10 mg/kg) or clorgyline (10 mg/kg). In the medial part of the central telencephalon, the nucleus telencephali, pars medialis, MPTP caused a decrease in the number of TH-immunoreactive neurons and distortions in their labelling pattern. Electron microscopic observations showed that MPTP caused swelling of cell processes, changes in neuronal nuclear profiles, dilation of endoplasmic reticulum, intracellular vacuolization and membrane distortions, and degeneration of neuronal fibers in this brain area. MPTP also caused a small reduction and some diffuseness in the labelling of dopaminergic neurons in several diencephalic periventricular nuclei. Moreover, MPTP induced cell swelling and degeneration in the subependymal cell layers along the forebrain ventricles. In all areas, L-deprenyl appeared to partially prevent the MPTP-induced degenerative changes. We conclude that in the goldfish MPTP causes marked histochemical changes in selected dopaminergic brain systems coincident with the Parkinson-like locomotor and neurochemical deficits.
Insights
The neurotoxin MPTP causes Parkinson-like symptoms in goldfish by damaging dopaminergic neurons. L-deprenyl treatment partially protected against these MPTP-induced neurotoxic effects.
Area of Science:
- Neuroscience
- Toxicology
- Comparative Neurology
Background:
- The neurotoxin MPTP induces Parkinsonism in various species.
- Goldfish (Carassius auratus) exhibit Parkinsonian symptoms after MPTP exposure, including bradykinesia and altered catecholamine levels.
Purpose of the Study:
- To investigate the histopathological effects of MPTP on dopaminergic neurons in the goldfish brain.
- To examine the protective role of L-deprenyl and clorgyline against MPTP-induced neurotoxicity.
Main Methods:
- Light and electron microscopy were used to assess changes in tyrosine hydroxylase (TH)-immunoreactive neurons.
- Goldfish were treated with MPTP, L-deprenyl, or clorgyline, and brain tissues were analyzed.
Main Results:
- MPTP decreased TH-immunoreactive neurons and altered their morphology in the telencephalon.
- Ultrastructural analysis revealed neuronal process swelling, nuclear changes, endoplasmic reticulum dilation, vacuolization, and fiber degeneration.
- MPTP also affected dopaminergic neurons in diencephalic nuclei and subependymal cells, with L-deprenyl showing partial protection.
Conclusions:
- MPTP induces significant histochemical and ultrastructural changes in goldfish dopaminergic systems.
- These changes correlate with Parkinson-like motor and neurochemical deficits observed in MPTP-treated goldfish.
- L-deprenyl demonstrates a partial neuroprotective effect against MPTP toxicity in this model.