PUBLICATION

Neuroprotective and neuro-restorative effects of minocycline and rasagiline in a zebrafish 6-hydroxydopamine model of Parkinson's disease

Authors
Cronin, A., Grealy, M.
ID
ZDB-PUB-171029-4
Date
2017
Source
Neuroscience   367: 34-46 (Journal)
Registered Authors
Grealy, Maura
Keywords
6-OHDA, Immunohistochemistry, Locomotor activity, Neuro-restoration, Parkinsons's disease, Zebrafish
MeSH Terms
  • Adrenergic Agents/toxicity
  • Analysis of Variance
  • Animals
  • Disease Models, Animal
  • Dopaminergic Neurons/drug effects*
  • Drug Administration Schedule
  • Embryo, Nonmammalian
  • Indans/therapeutic use*
  • Isradipine/therapeutic use
  • Levodopa/therapeutic use
  • Locomotion/drug effects
  • Minocycline/therapeutic use*
  • Neuroprotective Agents/therapeutic use*
  • Oxidopamine/toxicity
  • Parkinson Disease/drug therapy*
  • Parkinson Disease/etiology
  • Time Factors
  • Tyrosine 3-Monooxygenase/metabolism
  • Zebrafish
PubMed
29079063 Full text @ Neuroscience
Abstract
Parkinson's disease is a common, debilitating, neurodegenerative disorder for which the current gold standard treatment, levodopa (L-DOPA) is symptomatic. There is an urgent, unmet need for neuroprotective or, ideally, neuro-restorative drugs. We describe a 6-hydroxydopamine (6-OHDA) zebrafish model to screen drugs for neuroprotective and neuro-restorative capacity. Zebrafish larvae at two days post fertilization were exposed to 6-OHDA for three days, with co-administration of test drugs for neuroprotection experiments, or for 32 hours, with subsequent treatment with test drugs for neuro-restoration experiments. Locomotor activity was assessed by automated tracking and dopaminergic neurons were visualized by tyrosine hydroxylase immuno-histochemistry. Exposure to 6-OHDA for either 32 hours or 3 days induced similar, significant locomotor deficits and neuronal loss in 5 day-old larvae. L-DOPA (1 mM) partially restored locomotor activity, but was neither neuroprotective nor neuro-restorative, mirroring the clinical situation. The calcium channel blocker, isradipine (1 µM) did not prevent or reverse 6-OHDA induced locomotor deficit or neuronal loss. However, both the tetracycline analogue, minocycline (10 µM), and the monoamine oxidase B inhibitor, rasagiline (1 µM), prevented the locomotor deficits and neuronal loss due to three-day 6-OHDA exposure. Importantly, they also reversed the locomotor deficit caused by prior exposure to 6-OHDA; rasagiline also reversed neuronal loss and minocycline partially restored neuronal loss due to prior 6-OHDA, making them candidates for investigation as neuro-restorative treatments for Parkinson's disease. Our findings in zebrafish reflect preliminary clinical findings for rasagiline and minocycline. Thus, we have developed a zebrafish model suitable for high-throughput screening of putative neuroprotective and neuro-restorative therapies for the treatment of Parkinson's disease.
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