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Updated: May 28, 2026
09:39
Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
Published on: June 26, 2013
Mechanism for long-term memory formation when synaptic strengthening is impaired
Kasia Radwanska1, Nikolay I Medvedev, Grace S Pereira
1Institute of Psychiatry, King's College London, London SE5 9NU, United Kingdom.
Summary
Impaired synaptic strengthening in memory formation can lead to invariant long-term memory (LTM) through new synapse growth, driven by mammalian target of rapamycin (mTOR) signaling and PSD95 protein upregulation.
Area of Science:
- Neuroscience
- Molecular Biology
- Synaptic Plasticity
Background:
- Long-term memory (LTM) formation involves synaptic strengthening and synaptogenesis.
- The specific role of synaptogenesis in LTM formation remains unclear.
Purpose of the Study:
- To investigate whether synaptogenesis contributes to LTM formation when synaptic strengthening is impaired.
- To elucidate the molecular mechanisms underlying LTM formation under conditions of compromised synaptic plasticity.
Main Methods:
- Utilized alpha-calcium/calmodulin kinase II autophosphorylation-deficient (T286A) mutant mice.
- Assessed contextual LTM formation, PSD95 protein levels, and spine morphology post-training.
- Investigated the role of mammalian target of rapamycin (mTOR) signaling pathway.
Main Results:
- In T286A mutants with impaired functional strengthening, LTM formation correlated with PSD95 upregulation and persistent multi-innervated spine generation.
- Both PSD95 upregulation and LTM formation in these mutants were dependent on mTOR signaling.
- Contextual LTM in T286A mutants exhibited resistance to destabilization, indicating reduced flexibility.
Conclusions:
- Synaptogenesis, driven by mTOR signaling and PSD95 overexpression, contributes to the formation of invariant LTM when functional synaptic strengthening is impaired.
- Impaired synaptic strengthening leads to less flexible LTM.
- This study highlights a novel pathway for LTM formation characterized by structural synaptic changes.
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