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BDNF activates mTOR to regulate GluR1 expression required for memory formation.

Leandro Slipczuk1, Pedro Bekinschtein, Cynthia Katche

  • 1Instituto de Biología Celular y Neurociencias, Facultad de Medicina, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina.

Plos One
|June 24, 2009
PubMed
Summary
This summary is machine-generated.

Mammalian target of Rapamycin (mTOR) activation is crucial for long-term memory consolidation. This process involves BDNF signaling and regulates synaptic GluR1 expression for memory formation.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Signaling

Background:

  • The mammalian target of Rapamycin (mTOR) kinase regulates protein synthesis initiation, impacting synaptic plasticity and long-term memory (LTM).
  • While mTOR's role in LTM is established, its activation timeline and upstream regulators during memory processing remain unclear.

Purpose of the Study:

  • To investigate the temporal dynamics of mTOR activation during inhibitory avoidance (IA) long-term memory (LTM) consolidation.
  • To identify extracellular signals, specifically Brain-Derived Neurotrophic Factor (BDNF), that govern mTOR activation during memory formation.
  • To elucidate the downstream targets of mTOR signaling, such as GluR1, involved in LTM.

Main Methods:

  • In vivo assessment of mTOR activation in the dorsal hippocampus following IA training.
  • Administration of function-blocking anti-BDNF antibodies and BDNF antisense oligonucleotides (ASO) to investigate BDNF's role.
  • Measurement of GluR1 subunit expression and p70S6K phosphorylation as readouts of mTOR activity.
  • Utilized rapamycin-sensitive assays and ASO to block specific molecular pathways.

Main Results:

  • IA LTM consolidation involves biphasic mTOR activation in the dorsal hippocampus at training and 3 hours post-training.
  • BDNF signaling is essential for IA LTM retention, acting upstream of mTOR activation and p70S6K phosphorylation.
  • mTOR activation leads to a rapamycin-sensitive increase in synaptic GluR1 expression, critical for memory consolidation, and this increase is blocked by GluR1 ASO.

Conclusions:

  • mTOR-mediated translation is vital for memory consolidation within specific temporal windows.
  • BDNF acts as an upstream regulator of hippocampal mTOR signaling during fear memory consolidation.
  • mTOR signaling directly controls the upregulation of synaptic GluR1, a key molecular substrate for memory consolidation.