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Depotentiation Of Long-Term Potentiation Is Associated With Epitope-Specific Tau Hyper-/Hypophosphorylation In The Hippocampus Of Adult Rats
- Publication Year :
- 2019
- Publisher :
- Aperta, 2019.
-
Abstract
- It is well-known that some kinases which are involved in the induction of synaptic plasticity probably modulate tau phosphorylation. However, how depression of potentiated synaptic strength contributes to tau phosphorylation is unclear because of the lack of experiments in which depotentiation of LTP was induced. Field excitatory postsynaptic potential (fEPSP) and population spike (PS) were recorded from the dentate gyrus in response to the perforant pathway stimulation. To induce LTP, high-frequency stimulation (HFS) was used, while, for depotentiation of LTP, low-frequency stimulation (LFS) consisting of 900 pulses at 1 Hz was applied 5 min after tetanization. In some experiments, a neutral protocol at 0.033 Hz was applied throughout the experiment without any induction of synaptic plasticity. One-hertz depotentiation protocol was able to decrease fEPSP slope which was previously increased by HFS, whereas no significant change in fEPSP slope and PS amplitude was observed in neutral protocol experiments. Relative to saline infusion, LTP was lower in magnitude and was more reversed by subsequent LFS in the presence of ERK1/2 inhibitor. Western blot experiments indicated that tau protein was hyperphosphorylated at ser416 epitope but rather hypophosphorylated at thr231 epitope in the whole hippocampus upon depotentiation of LTP. These changes concomitantly occurred with a notable increase in the levels of total tau and in the levels of phosphorylated form of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). ERK1/2 inhibition resulted in a decrease in phosphorylation of tau at p416Tau when ERK1/2 was inhibited. These findings indicate that some forms of long-term plastic changes might be related with epitope-specific tau phosphorylation and ERK1/2 activation in the hippocampus. Therefore, we emphasize that tau may be crucial for physiological learning as well as Alzheimer's disease pathology.
- Subjects :
- Male
0301 basic medicine
Amino Acid Motifs
Long-Term Potentiation
Tau protein
Hippocampus
tau Proteins
03 medical and health sciences
Cellular and Molecular Neuroscience
0302 clinical medicine
Animals
Phosphorylation
Rats, Wistar
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
biology
Chemistry
Dentate gyrus
Excitatory Postsynaptic Potentials
Long-term potentiation
Population spike
General Medicine
Rats
Cell biology
030104 developmental biology
Synaptic plasticity
Excitatory postsynaptic potential
biology.protein
Depotentiation
Protein Processing, Post-Translational
030217 neurology & neurosurgery
Subjects
Details
- Database :
- OpenAIRE
- Accession number :
- edsair.doi.dedup.....c5f2deb9fe6677d97ca455fb65648e6c