Molecular mechanisms contributing to long-lasting synaptic plasticity at the 
temporoammonic-CA1 synapse

Remondes, M.; Schuman, Erin M.

doi:10.1101/lm.59103

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Molecular mechanisms contributing to long-lasting synaptic plasticity at the temporoammonic-CA1 synapse

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Schuman, Erin M.
Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/12888542
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Citation

Remondes, M., & Schuman, E. M. (2003). Molecular mechanisms contributing to long-lasting synaptic plasticity at the temporoammonic-CA1 synapse. Learn Mem, 10(4), 247-52. doi:10.1101/lm.59103.

Cite as: http://hdl.handle.net/21.11116/0000-0007-EF72-C

Abstract

The hippocampus and the nearby medial temporal lobe structures are required for the formation, consolidation, and retrieval of episodic memories. Sensory information enters the hippocampus via two inputs from entorhinal cortex (EC): One input (perforant path) makes synapses on the dendrites of dentate granule cells as the first set of synapses in the trisynaptic circuit, the other (temporoammonic; TA) makes synapses on the distal dendrites of CA1 neurons. Here we demonstrate that TA-CA1 synapses undergo both early- and late-phase long-term potentiation (LTP) in rat hippocampal slices. LTP at TA-CA1 synapses requires both NMDA receptor and voltage-gated Ca2+ channel activity. Furthermore, TA-CA1 LTP is insensitive to the blockade of fast inhibitory transmission (GABAA-mediated) and, interestingly, is dependent on GABAB-dependent slow inhibitory transmission. These findings indicate that the TA-CA1 synapses may rely on a refined modulation of inhibition to exhibit LTP.