The role of passive normalization, voltage-gated channels and synaptic scaling in site-independence of somatic EPSP amplitude in CA1 pyramidal neurons

Abstract Dendrites of pyramidal cells receive excitatory synapses and attenuate them toward the soma. “Synaptic attenuation” in CA1 pyramidal cells is compensated with “synaptic scaling” to make the amplitude of somatically recorded EPSPs site-independent. Recent studies, however, show that voltage-gated channels and passive properties of dendrites have impact on the sub-threshold EPSP amplitude. In this study, we want to evaluate the relative importance of three factors on site-independence of somatic EPSP amplitude: (1) “passive normalization” in non-uniform passive models, (2) voltage-gated channels which are active in the resting membrane potential, and (3) synaptic scaling. Using modeling method, we show that in the first 3/4 of apical dendrite, synaptic scaling rule can make somatic EPSPs location-independent, but role of passive-normalization is limited in this process. Also, we show that addition of voltage-gated conductances to a passive model reduces its excitability generally, and that M-type potassium ( I M ) currents increase the synaptic scaling degree, but persistent sodium current ( I NaP ) decrease it. The counterbalancing effects of these somatic channels, mostly affect the synaptic scaling in the distal apical dendrites, and are not feasible in the absence of hyperpolarization activated current ( I h ). Increasing I h density, however, has paradoxical effects on synaptic scaling; dEPSP amplitude diminishes while synaptic weight increases.