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Updated: Jun 8, 2026
05:28
A Semi-Quantitative Drug Affinity Responsive Target Stability (DARTS) assay for studying Rapamycin/mTOR interaction
Published on: August 27, 2019
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
Summary
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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