Journal of Neuroscience, Vol 12, 607-618, Copyright © 1992 by Society for Neuroscience
Computer simulations of EPSP-spike (E-S) potentiation in hippocampal CA1 pyramidal cells
JC Wathey, WW Lytton, JM Jester and TJ Sejnowski
Computational Neurobiology Laboratory, Salk Institute for Biological Studies, San Diego, California 92186-5800.
Long-term potentiation of hippocampal excitatory synapses is often
accompanied by an increase in the probability of spiking to an EPSP of
fixed strength (E-S potentiation). We used computer simulations of a CA1
pyramidal neuron to test the plausibility of the hypothesis that E- S
potentiation is caused by changes in dendritic excitability. These changes
were simulated by adding "hot spots" of noninactivating voltage- sensitive
Ca2+ conductance to various dendritic compartments. This typically caused
spiking in response to previously subthreshold synaptic inputs. The
magnitude of the simulated E-S potentiation depended on the passive
electrical properties of the cell, the excitability of the soma, and the
relative locations on the dendrites of the synaptic inputs and hot spots.
The specificity of the simulated E-S potentiation was quantified by
colocalizing the hot spots with a subset (40 of 80) of the synaptic
contacts, denoted "tetanized," and then comparing the effects of the hot
spots on these and the remaining (untetanized) synaptic contacts. The
simulated E-S potentiation tended to be specific to the tetanized input if
the untetanized contacts were, on average, electrically closer to the soma
than the tetanized contacts. Specificity was also high if the tetanized and
untetanized contacts were segregated to different primary dendrites. The
results also predict, however, that E-S potentiation by this mechanism will
appear to be nonspecific (heterosynaptic) if the synapses of the
untetanized input are sufficiently far from the soma relative to the
tetanized synapses. Experimental confirmation of this prediction would
support the hypothesis that changes in postsynaptic excitability can
contribute to hippocampal E-S potentiation.