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Long-term Potentiation01:35

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term Potentiation01:25

Long-term Potentiation

3.2K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
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Related Experiment Video

Updated: Dec 13, 2025

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
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Synaptic RTP801 contributes to motor-learning dysfunction in Huntington's disease.

Núria Martín-Flores1,2, Leticia Pérez-Sisqués3,4, Jordi Creus-Muncunill3,4,5,6

  • 1Department of Biomedicine, Faculty of Medicine, University of Barcelona, 08036, Barcelona, Catalonia, Spain. nuria.martinfl21@gmail.com.

Cell Death & Disease
|August 1, 2020
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Summary

Stress-responsive RTP801 (also known as REDD1) protein contributes to mutant huntingtin toxicity and motor deficits in Huntington

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • RTP801/REDD1 is a stress-responsive protein implicated in mutant huntingtin (mhtt) toxicity.
  • RTP801 levels are elevated in the putamen of Huntington's disease (HD) patients.

Purpose of the Study:

  • To investigate the role of RTP801 in striatal synaptic plasticity and motor impairment in Huntington's disease (HD).

Main Methods:

  • Overexpression of ectopic mhtt in cultured rat neurons.
  • Assessment of RTP801 protein levels in human postmortem HD brains and HD mouse models.
  • Striatal RTP801 knockdown using adeno-associated viral vectors in R6/1 HD mice.
  • Evaluation of motor learning in treated mice.

Main Results:

  • Ectopic mhtt increased RTP801 in neuronal synapses.
  • RTP801 was upregulated in striatal synapses of HD patients and mouse models.
  • RTP801 knockdown in R6/1 mice ameliorated motor-learning deficits.
  • Silencing RTP801 normalized Akt hyperphosphorylation and increased synaptic GluA1 and TrkB levels, enhancing synaptic plasticity.

Conclusions:

  • Mutant huntingtin-induced RTP801 mediates motor dysfunction in HD models.
  • RTP801 plays a role in the pathophysiology of Huntington's disease.
  • Targeting the RTP801/Akt/mTOR pathway offers a potential therapeutic strategy for HD.