Biophysical Model of a Hebbian Synapse
- Creators
- Zador, Anthony
-
Koch, Christof
- Brown, Thomas H.
Abstract
We present a biophysical model of electrical and Ca(2+) dynamics following activation of N-methyl-D-aspartate (NMDA) receptors located on a dendritic spine. The model accounts for much of the phenomenology of the induction of long-term potentiation at a Hebbian synapse in hippocampal region CA1. Computer simulations suggested four important functions of spines in this Ca(^2+)-dependent synaptic modification: (i) compartmentalizing transient changes in [Ca(2+)] to just those synapses that satisfy the conjunctive requirement for synaptic modification; (ii) isolating the spine head from changes in the [Ca(2+)] at the dendritic shaft; (iii) amplifying the concentration changes at those synapses; and (iv) increasing the voltage dependence of the processes underlying long term potentiation induction. This proposed role of spines in the regulation of Ca(^2+) dynamics contrasts with traditional approaches to spine function that have stressed electronic properties. This model can be used to explore the computational implications of Hebbian synapses.
Additional Information
Communicated by Francis Crick, May 25, 1990. We thank Dr. Francis Crick for useful discussions, Dr. C. F. Stevens for making experimental results available before publication, and Ms. Anna C. Nobre for comments on the manuscript. This research was supported by grants from the Office of Naval Research and the Defense Advanced Research Projects Agency.Attached Files
Published - PNAS-1990-Zador-6718-22.pdf
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Additional details
- PMCID
- PMC54608
- Eprint ID
- 40549
- Resolver ID
- CaltechAUTHORS:20130816-103239387
- U.S. Office of Naval Research
- Defense Advanced Research Projects Agency
- Created
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2008-01-26Created from EPrint's datestamp field
- Updated
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2020-03-03Created from EPrint's last_modified field
- Caltech groups
- Koch Laboratory (KLAB)