Neuroscience 2005 Abstract
| Presentation Number: | 735.9 |
|---|---|
| Abstract Title: | Schaffer collateral input modulates temporoammonic input to hippocampal CA1 pyramidal neurons: a computer simulation study. |
| Authors: |
Lazarewicz, M. T.*1
; Ang, C. W.1,3
; Carlson, G. C.3
; Coulter, D. A.1,2,3
; Finkel, L. H.1
1Bioengineering, Univ. of Pennsylvania, Philadelphia, PA 2Pediatrics and Neuroscience, Univ. of Pennsylvania, Philadelphia, PA 3PA, 120 Hayden Hall, 19104, |
| Primary Theme and Topics |
Neural Excitability, Synapses, and Glia: Cellular Mechanisms - Network interactions -- Signal propagation |
| Secondary Theme and Topics | Disorders of the Nervous System<br />- Epilepsy<br />-- Basic mechanisms |
| Session: |
735. Signal Propagation I Poster |
| Presentation Time: | Tuesday, November 15, 2005 1:00 PM-2:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # S11 |
| Keywords: | NMDA, VSD, OPTICAL IMAGING, EPILEPSY |
In hippocampal CA1 pyramidal neurons, the distal apical tuft receives inputs from entorhinal cortex via the temporoammonic (TA) pathway. Though electrotonically distant from the cell soma, TA inputs have been shown to influence hippocampal place cell firing.
Using a morphologically accurate compartmental model we were able to replicate results of previously reported voltage sensitive dye imaging studies (Ang, Carlson, & Coulter, SFN, 853.1, 2004) showing that local circuit activity shapes the effect of TA inputs into area CA1. Specifically we were able to show following three features: 1) Burst stimulation in the stratum lacunosum moleculare evoked EPSPs spatially restricted to the TA pathway. 2) Removal of GABAA inhibition significantly increased TA throughput to the cell soma. 3) When burst stimulation in the stratum lacunosum moleculare is preceded (40 ms) by excitatory input to Shaffer collateral afferents, TA throughput to the cell soma is significantly increased.
In the model, the TA input triggers dendritic spikes in apical dendrites that are shunted at their proximal shafts by feedforward GABAergic inputs. Schaffer collaterals open GABA and NMDA receptors simultaneously, introducing a bistable membrane voltage state in the apical tree. When this occurs in a time window just before the TA stimulation, some dendritic spikes are widened and strengthened sufficiently to overcome the proximal inhibition, allowing TA throughput to the cell soma. Thus the timing of the Schaffer collateral input gates TA throughput to the cell soma.
Using a morphologically accurate compartmental model we were able to replicate results of previously reported voltage sensitive dye imaging studies (Ang, Carlson, & Coulter, SFN, 853.1, 2004) showing that local circuit activity shapes the effect of TA inputs into area CA1. Specifically we were able to show following three features: 1) Burst stimulation in the stratum lacunosum moleculare evoked EPSPs spatially restricted to the TA pathway. 2) Removal of GABAA inhibition significantly increased TA throughput to the cell soma. 3) When burst stimulation in the stratum lacunosum moleculare is preceded (40 ms) by excitatory input to Shaffer collateral afferents, TA throughput to the cell soma is significantly increased.
In the model, the TA input triggers dendritic spikes in apical dendrites that are shunted at their proximal shafts by feedforward GABAergic inputs. Schaffer collaterals open GABA and NMDA receptors simultaneously, introducing a bistable membrane voltage state in the apical tree. When this occurs in a time window just before the TA stimulation, some dendritic spikes are widened and strengthened sufficiently to overcome the proximal inhibition, allowing TA throughput to the cell soma. Thus the timing of the Schaffer collateral input gates TA throughput to the cell soma.
Supported by NIH NS 41811
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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