Home > Publications Database > Pro-aggregant Tau impairs mossy fiber plasticity due to structural changes and Ca(++) dysregulation. > print

001     138082
005     20240601120430.0
024 7 _ |a 10.1186/s40478-015-0193-3
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024 7 _ |a pmc:PMC4384391
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037 _ _ |a DZNE-2020-04404
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Decker, Jochen Martin
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245 _ _ |a Pro-aggregant Tau impairs mossy fiber plasticity due to structural changes and Ca(++) dysregulation.
260 _ _ |a London
|c 2015
|b Biomed Central
264 _ 1 |3 online
|2 Crossref
|b Springer Science and Business Media LLC
|c 2015-04-03
264 _ 1 |3 print
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|b Springer Science and Business Media LLC
|c 2015-12-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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520 _ _ |a We used an inducible mouse model expressing the Tau repeat domain with the pro-aggregant mutation ΔK280 to analyze presynaptic Tau pathology in the hippocampus.Expression of pro-aggregant Tau(RDΔ) leads to phosphorylation, aggregation and missorting of Tau in area CA3. To test presynaptic pathophysiology we used electrophysiology in the mossy fiber tract. Synaptic transmission was severely disturbed in pro-aggregant Tau(RDΔ) and Tau-knockout mice. Long-term depression of the mossy fiber tract failed in pro-aggregant Tau(RDΔ) mice. We observed an increase in bouton size, but a decline in numbers and presynaptic markers. Both pre-and postsynaptic structural deficits are preventable by inhibition of Tau(RDΔ) aggregation. Calcium imaging revealed progressive calcium dysregulation in boutons of pro-aggregant Tau(RDΔ) mice. In N2a cells we observed this even in cells without tangle load, whilst in primary hippocampal neurons transient Tau(RDΔ) expression alone caused similar Ca(++) dysregulation. Ultrastructural analysis revealed a severe depletion of synaptic vesicles pool in accordance with synaptic transmission impairments.We conclude that oligomer formation by Tau(RDΔ) causes pre- and postsynaptic structural deterioration and Ca(++) dysregulation which leads to synaptic plasticity deficits.
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650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 7 |a Calcium
|0 SY7Q814VUP
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Calcium: physiology
|2 MeSH
650 _ 2 |a Calcium Signaling: physiology
|2 MeSH
650 _ 2 |a Cell Culture Techniques
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Electrophysiology
|2 MeSH
650 _ 2 |a Hippocampus: physiology
|2 MeSH
650 _ 2 |a Long-Term Potentiation: physiology
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Mossy Fibers, Hippocampal: physiology
|2 MeSH
650 _ 2 |a Neuronal Plasticity: physiology
|2 MeSH
650 _ 2 |a Synaptic Transmission: physiology
|2 MeSH
650 _ 2 |a tau Proteins: deficiency
|2 MeSH
650 _ 2 |a tau Proteins: genetics
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
700 1 _ |a Krüger, Lars
|0 P:(DE-2719)2810335
|b 1
|u dzne
700 1 _ |a Sydow, Astrid
|0 P:(DE-2719)2810788
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700 1 _ |a Zhao, Shanting
|b 3
700 1 _ |a Frotscher, Michael
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700 1 _ |a Mandelkow, Eckhard
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700 1 _ |a Mandelkow, Eva-Maria
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773 1 8 |a 10.1186/s40478-015-0193-3
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|t Acta Neuropathologica Communications
|v 3
|y 2015
|x 2051-5960
773 _ _ |a 10.1186/s40478-015-0193-3
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856 4 _ |y OpenAccess
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