PGE 2 -EP3 signaling pathway impairs hippocampal presynaptic long-term plasticity in a mouse model of Alzheimer's disease
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by early cognitive deficits linked to synaptic dysfunction and loss. Considerable evidence suggests that neuroinflammation contributes to AD. Prostaglandin E (PGE ), a key neuroinflammatory molecule, modulates hip...
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| Published in | Neurobiology of aging Vol. 50; pp. 13 - 24 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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United States
01.02.2017
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| Abstract | Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by early cognitive deficits linked to synaptic dysfunction and loss. Considerable evidence suggests that neuroinflammation contributes to AD. Prostaglandin E
(PGE
), a key neuroinflammatory molecule, modulates hippocampal synaptic transmission and plasticity. We investigated the effect of PGE
on synaptic transmission and presynaptic plasticity at synapses between mossy fibers from the dentate gyrus and CA3 pyramidal cells (Mf-CA3 synapse). These synapses are involved in mnemonic processes and consequently may be of relevance for AD. We provide evidence that although PGE
had no effect both on either basal transmission or short-term plasticity, it strongly impaired presynaptic Mf-CA3 long-term potentiation (LTP) by acting on PGE
receptor 3 (EP3) receptors. During aging, hippocampal levels of PGE
markedly increased in the APP/PS1 mouse model of AD and impaired specifically presynaptic LTP via a PGE
-EP3 signaling pathway. In summary, the building up of PGE
during the progression of AD leads to specific impairment of hippocampal presynaptic plasticity and highlights EP3 receptors as a potential target to alleviate cognitive deficits in AD. |
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| AbstractList | Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by early cognitive deficits linked to synaptic dysfunction and loss. Considerable evidence suggests that neuroinflammation contributes to AD. Prostaglandin E
(PGE
), a key neuroinflammatory molecule, modulates hippocampal synaptic transmission and plasticity. We investigated the effect of PGE
on synaptic transmission and presynaptic plasticity at synapses between mossy fibers from the dentate gyrus and CA3 pyramidal cells (Mf-CA3 synapse). These synapses are involved in mnemonic processes and consequently may be of relevance for AD. We provide evidence that although PGE
had no effect both on either basal transmission or short-term plasticity, it strongly impaired presynaptic Mf-CA3 long-term potentiation (LTP) by acting on PGE
receptor 3 (EP3) receptors. During aging, hippocampal levels of PGE
markedly increased in the APP/PS1 mouse model of AD and impaired specifically presynaptic LTP via a PGE
-EP3 signaling pathway. In summary, the building up of PGE
during the progression of AD leads to specific impairment of hippocampal presynaptic plasticity and highlights EP3 receptors as a potential target to alleviate cognitive deficits in AD. |
| Author | Barthet, Gaël Maingret, Vincent Deforges, Séverine Amédée, Thierry Jiang, Nan Mulle, Christophe |
| Author_xml | – sequence: 1 givenname: Vincent surname: Maingret fullname: Maingret, Vincent organization: Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, Bordeaux, France; University of Bordeaux, Bordeaux, France – sequence: 2 givenname: Gaël surname: Barthet fullname: Barthet, Gaël organization: Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, Bordeaux, France; University of Bordeaux, Bordeaux, France – sequence: 3 givenname: Séverine surname: Deforges fullname: Deforges, Séverine organization: Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, Bordeaux, France; University of Bordeaux, Bordeaux, France – sequence: 4 givenname: Nan surname: Jiang fullname: Jiang, Nan organization: Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, Bordeaux, France; University of Bordeaux, Bordeaux, France – sequence: 5 givenname: Christophe surname: Mulle fullname: Mulle, Christophe organization: Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, Bordeaux, France; University of Bordeaux, Bordeaux, France – sequence: 6 givenname: Thierry surname: Amédée fullname: Amédée, Thierry email: thierry.amedee@u-bordeaux.fr organization: Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, Bordeaux, France; University of Bordeaux, Bordeaux, France. Electronic address: thierry.amedee@u-bordeaux.fr |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27837675$$D View this record in MEDLINE/PubMed |
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| Keywords | Inflammation Alzheimer's disease APP/PS1 Hippocampus Synaptic plasticity PGE |
| Language | English |
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| SubjectTerms | Aging - metabolism Aging - physiology Alzheimer Disease - etiology Alzheimer Disease - therapy Animals Dinoprostone - physiology Disease Models, Animal Hippocampus - physiopathology Long-Term Potentiation Male Mice, Inbred C57BL Mice, Transgenic Molecular Targeted Therapy Neuronal Plasticity - genetics Neuronal Plasticity - physiology Receptors, Prostaglandin E, EP3 Subtype - physiology Signal Transduction - physiology Synapses - physiology Synaptic Transmission - genetics Synaptic Transmission - physiology |
| Title | PGE 2 -EP3 signaling pathway impairs hippocampal presynaptic long-term plasticity in a mouse model of Alzheimer's disease |
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