Faculty Mentor(s)

Dr. Erika Calvo-Ochoa, Biology

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Parkinson's disease is a neurodegenerative disorder caused by degeneration of dopaminergic neurons, and an early symptom of Parkinson's disease is olfactory dysfunction. A common animal model used in Parkinson's disease research is zebrafish because of their unique neuro-regenerative ability, which is particularly in their olfactory bulb. In order to create a model of the early stages of Parkinson's disease we injected zebrafish with the neurotoxin 6-hydroxydopamine (6-OHDA) to induce the degeneration of dopaminergic neurons in the olfactory bulb. Olfactory system recovery post 6-OHDA injection has been recorded in previous literature, but the state of synaptic dopaminergic synapses post-injection has not yet been investigated. In this study, we explore the effects of 6OH-DA lesions on dopaminergic neuron number and synaptic density within the olfactory bulbs of control and experimental samples at 1- and 3-days post 6-OHDA injection. For this, we harvested zebrafish brains post-injection and performed immunohistochemical staining on the neural tissue. We used primary antibodies against SV2 (synaptic vesicle 2) and TH (tyrosine hydroxylase) that allowed us to observe pre-synaptic terminals of dopaminergic neurons, respectively, as well as their overlap. We observed the tissue using confocal microscopy, measured the optical density of the signal, and counted the number of dopaminergic neurons present within each tissue sample. So far, we have qualitatively observed differences in the location of the synaptic vesicles and olfactory glomeruli (i.e., sites of synaptic connections) between treatment groups. Our research is the first to examine dopaminergic synapse loss resulting from treatment with 6-OHDA, and may give insight into preventative treatments of neurodegenerative disorders like Parkinson's disease in the future.


This research was supported by the Neuroscience program and Biology Department of Hope College.