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  • Florey Department of Neuroscience and Mental Health
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    Pramipexole restores depressed transmission in the ventral hippocampus following MPTP-lesion

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    Author
    Castro-Hernandez, J; Adlard, PA; Finkelstein, DI
    Date
    2017-03-14
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Finkelstein, David; Adlard, Paul
    Affiliation
    Florey Department of Neuroscience and Mental Health
    Metadata
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    Document Type
    Journal Article
    Citations
    Castro-Hernandez, J., Adlard, P. A. & Finkelstein, D. I. (2017). Pramipexole restores depressed transmission in the ventral hippocampus following MPTP-lesion. SCIENTIFIC REPORTS, 7 (1), https://doi.org/10.1038/srep44426.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258383
    DOI
    10.1038/srep44426
    Abstract
    The hippocampus has a significant association with memory, cognition and emotions. The dopaminergic projections from both the ventral tegmental area and substantia nigra are thought to be involved in hippocampal activity. To date, however, few studies have investigated dopaminergic innervation in the hippocampus or the functional consequences of reduced dopamine in disease models. Further complicating this, the hippocampus exhibits anatomical and functional differentiation along its dorso-ventral axis. In this work we investigated the role of dopamine on hippocampal long term potentiation using D-amphetamine, which stimulates dopamine release, and also examined how a dopaminergic lesion affects the synaptic transmission across the anatomic subdivisions of the hippocampus. Our findings indicate that a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine induced dopaminergic lesion has time-dependent effects and impacts mainly on the ventral region of the hippocampus, consistent with the density of dopaminergic innervation. Treatment with a preferential D3 receptor agonist pramipexole partly restored normal synaptic transmission and Long-Term Potentiation. These data suggest a new mechanism to explain some of the actions of pramipexole in Parkinson´s disease.

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