ArticleProceedings of the National Academy of Sciences of the United States of America2007
1-Methyl-4-phenylpyridinium induces synaptic dysfunction through a pathway involving caspase and PKCdelta enzymatic activities.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Protein Kinase C-delta (PKCδ) in Neurodegeneration and Cerebral Ischemia: Molecular Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Doxycycline inhibits dopaminergic neurodegeneration through upregulation of axonal and synaptic proteins.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Engagement of Neurotropic Viruses in Fast Axonal Transport: Mechanisms, Potential Role of Host Kinases and Implications for Neuronal Dysfunction.Frontiers in cellular neuroscience · 2021Article
- Peripheral Administration of Tetanus Toxin Hc Fragment Prevents MPPNeurotoxicity research · 2018Article
- Regulation of motor proteins, axonal transport deficits and adult-onset neurodegenerative diseases.Neurobiology of disease · 2017Review
- Prion protein inhibits fast axonal transport through a mechanism involving casein kinase 2.PloS one · 2017Article
- The neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) alters hippocampal excitatory synaptic transmission by modulation of the GABAergic system.Frontiers in cellular neuroscience · 2015Article
- Axon degeneration in Parkinson's disease.Experimental neurology · 2013Review
- Alterations in axonal transport motor proteins in sporadic and experimental Parkinson's disease.Brain : a journal of neurology · 2012Article
- Blocking Effects of Human Tau on Squid Giant Synapse Transmission and Its Prevention by T-817 MA.Frontiers in synaptic neuroscience · 2011Article
- A perspective on neuronal cell death signaling and neurodegeneration.Molecular neurobiology · 2010Article
- Polyunsaturated fatty acids protect against prion-mediated synapse damage in vitro.Neurotoxicity research · 2010Article
- Functional heterogeneity at dopamine release sites.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Axonal transport defects in neurodegenerative diseases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Review
- 1-Methyl-4-phenylpyridinium affects fast axonal transport by activation of caspase and protein kinase C.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration has been used, in various mammalian species, as an experimental model of Parkinson's disease. The pathogenesis for such pharmacologically induced Parkinson's disease involves 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. This metabolite produces rapid degeneration of nigrostriatal dopaminergic neurons, which causes the parkinsonian syndrome. In this work, we show that injection of MPP+ into the presynaptic terminal of the squid giant synapse blocks synaptic transmission without affecting the presynaptic action potential or the presynaptic calcium currents. These effects of MPP+ were mimicked by the injection of an active form of caspase-3 and prevented by inhibitors of caspase-3 and protein kinase C delta. Ultrastructurally, MPP+-injected synapses showed a dramatic reduction in the number of neurotransmitter vesicles at the presynaptic active zone, as compared with control synapses. Otherwise, normal docking and clathrin-coated vesicles were observed, albeit at much reduced numbers. These results indicate that MPP+ acutely reduces presynaptic vesicular availability, not release, and that MPP+-induced pathogenesis results from presynaptic dysfunction that leads, secondarily, to dying-back neuropathy in affected neurons.
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