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A Semi-Quantitative Drug Affinity Responsive Target Stability (DARTS) assay for studying Rapamycin/mTOR interaction
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mTOR inhibitor rapamycin suppresses striatal post-ischemic LTP

Veronica Ghiglieri1, Valentina Pendolino, Vincenza Bagetta

  • 1Fondazione Santa Lucia - IRCCS, via del Fosso di Fiorano, 64, 00143, Rome, Italy.

Experimental Neurology
|September 22, 2010
PubMed

Insights

The mammalian target of rapamycin (mTOR) pathway is crucial for a pathological brain plasticity called i-LTP. Inhibiting mTOR with rapamycin selectively blocks i-LTP, offering a potential therapy for ischemic brain injury.

Area of Science:

  • Neuroscience
  • Molecular Biology

Background:

  • The mammalian target of rapamycin (mTOR) pathway, comprising mTORC1 and mTORC2, integrates cellular signals.
  • Post-ischemic long-term potentiation (i-LTP) is a pathological plasticity in striatal medium spiny neurons (MSNs) following ischemia.

Purpose of the Study:

  • To investigate the role of mTOR complexes in the induction of i-LTP.
  • To assess the therapeutic potential of mTOR inhibition in ischemic conditions.

Main Methods:

  • Intracellular recordings of MSNs in corticostriatal slices.
  • Application of the mTOR inhibitor rapamycin (1μM) during in vitro ischemia.
  • Analysis of membrane depolarization and i-LTP induction.

Main Results:

  • Rapamycin did not alter ischemia-induced membrane depolarization.
  • Rapamycin completely prevented the induction of i-LTP.
  • Normal activity-dependent long-term potentiation (LTP) remained unaffected.

Conclusions:

  • mTOR signaling plays a critical role in i-LTP.
  • Selective blockade of i-LTP by rapamycin suggests a therapeutic strategy against ischemic brain damage.

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