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Updated: Jul 28, 2026
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
PKC activation rescues LTP from NMDA receptor blockade.
A M Kleschevnikov1, A Routtenberg
1Cresap Neuroscience Laboratory, Northwestern University Institute for Neuroscience, Evanston, Illinois 60208, USA.
Hippocampus
|May 10, 2001
Summary
Directly activating protein kinase C (PKC) can rescue long-term potentiation (LTP) blockade caused by NMDA receptor antagonists, supporting the synaptic dialogue hypothesis in neuroscience.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Molecular Biology
Background:
- Long-term potentiation (LTP) is crucial for learning and memory.
- The synaptic dialogue hypothesis proposes presynaptic protein kinase C (PKC) activation is key to LTP.
- NMDA receptor antagonists block LTP, but their effect on PKC is unclear.
Purpose of the Study:
- To test if direct PKC activation rescues LTP blockade by NMDA receptor antagonists.
- To investigate the role of presynaptic PKC in LTP expression.
Main Methods:
- Extracellular field excitatory postsynaptic potentials (fEPSPs) were recorded in the mouse dentate gyrus.
- Perforant path stimulation was used to induce LTP.
- Mice received infusions of vehicle, NMDA receptor antagonist APV, or APV with PKC activator PDBu.
Main Results:
- APV significantly suppressed LTP.
- Co-administration of APV and PDBu restored LTP to control levels.
- Reduced paired-pulse facilitation, indicating presynaptic involvement, was observed when LTP was present.
Conclusions:
- Presynaptic PKC activation can overcome NMDA receptor antagonist-induced blockade of LTP.
- This supports the synaptic dialogue hypothesis.
- Growth-associated protein GAP-43 may be a presynaptic target of PKC in LTP.
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