BIOPHYSICAL MODEL OF A HEBBIAN SYNAPSE

We present a biophysical model of electrical and Ca2+ 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 Ca2+-dependent synaptic modification: (i) compartmentalizing transient changes in [Ca2+] to just those synapses that satisfy the conjunctive requirement for synaptic modification; (ii) isolating the spine head from changes in the [Ca2+] 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 Ca2+ dynamics contrasts with traditional approaches to spine function that have stressed electrotonic properties. This model can be used to explore the computational implications of Hebbian synapses.