Abstract
CA1 pyramidal cells (PCs) provide a major output of the hippocampus proper. They integrate information arriving directly from the entorhinal cortex via the temporoammonic pathway, and indirectly via the polysynaptic dentate gyrus–CA3–CA1 loop. Both pathways terminate in a spatially segregated manner onto CA1 PC apical dendrites. The temporoammonic pathway targets the distal dendrites in the stratum lacunosum moleculare, while CA3 PC axons terminate within the stratum radiatum. These inputs are integrated in the somatodendritic compartment and converted to an output consisting of action potentials propagating along the CA1 axons, a process controlled by the intrinsic membrane properties of CA1 neurons. We will first consider the mechanisms determining input–output properties of normal CA1 PCs. We will then address how the properties of CA1 PCs change in acute and chronic epilepsy models, and how they might contribute to increased excitability.
Original language | English |
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Title of host publication | Encyclopedia of Basic Epilepsy Research |
Publisher | Elsevier |
Pages | 1272-1277 |
Number of pages | 6 |
ISBN (Electronic) | 9780123739612 |
DOIs | |
State | Published - 1 Jan 2009 |
Bibliographical note
Publisher Copyright:© 2009 Elsevier Ltd. All rights reserved.
Keywords
- Acute models of epilepsy
- AHP)
- CA1 pyramidal cells
- Epileptogenesis
- High K
- Intrinsic bursting
- Intrinsic excitability
- Kindling
- Low Ca
- Low Mg
- Osmotic pressure
- Spike afterpotentials (ADP
- Spike backpropagation
- Status epilepticus
- Subthreshold conductances (persistent Na current, T-type Ca current, M-type K current, A-type K current)
- Synchronization
- Transcriptional regulation