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Published on: January 10, 2015
Direct cortical inputs erase long-term potentiation at Schaffer collateral synapses
Yukitoshi Izumi1, Charles F Zorumski
1Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Cortical input to the hippocampus can reset synaptic potentiation (LTP) at Schaffer collateral synapses via adenosine A(1) receptors, facilitating new memory formation.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Hippocampal Function
Background:
- Long-term potentiation (LTP) at hippocampal Schaffer collateral (SC) synapses is crucial for memory.
- The role of direct entorhinal cortex input via the perforant path (PP) to CA1 is less understood.
Purpose of the Study:
- To investigate the effect of perforant path stimulation on Schaffer collateral synaptic transmission in the hippocampus.
- To elucidate the mechanisms underlying synaptic plasticity modulation by cortical inputs.
Main Methods:
- Low-frequency stimulation (LFS) of PP inputs to CA1.
- Electrophysiological recordings to assess basal SC transmission and LTP.
- Investigating the involvement of NMDA receptors, metabotropic glutamate receptors, calcium channels, and adenosine receptors.
Main Results:
- LFS of PP inputs did not affect basal SC transmission.
- LFS of PP inputs effectively depotentiated established SC LTP.
- This depotentiation was reversible by high-frequency stimulation of SC inputs.
- Depotentiation involved adenosine acting at A(1) receptors, independent of NMDA, group I mGluRs, or L-type Ca2+ channels.
Conclusions:
- Hippocampal synaptic plasticity can be modulated by cortical inputs.
- Adenosine A(1) receptor-mediated depotentiation of SC synapses provides a mechanism for resetting synaptic strength.
- This process may facilitate information processing and memory consolidation in the hippocampus.
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