Amplification of EPSPs by low Ni(2+)- and amiloride-sensitive Ca2+ channels in apical dendrites of rat CA1 pyramidal neurons.

Distal synaptic input to hippocampal CA1 pyramidal neurons was evoked by electrical stimulation of afferent fibers in outer stratum radiatum. Whole cell recordings from CA1 cell somata served to monitor excitatory postsynaptic potential (EPSP) envelopes after dendritic processing. To probe a functional role of low-voltage-activated Ca2+ current [or T current I(T)] in the apical dendrite, EPSP recordings were combined with local application of antagonists of I(T). Dendritic application of low concentrations of Ni2+ (5 microM) and amiloride (50 microM) reduced EPSP amplitude measured at the soma (resting membrane potential -70 mV) by 33.0 +/- 2.9% (mean +/- SE, n = 27) and 27.0 +/- 2.1% (n = 26), respectively. No appreciable effect on EPSP time course was observed. As expected from the voltage dependence of I(T) activation, the inhibitory effect of both antagonists was strongly attenuated when EPSPs were recorded at hyperpolarized membrane potential (-90 mV). In contrast to dendritic application, somatic application of Ni2+ or amiloride produced only weak reduction of EPSP amplitude. Our data indicate that dendritic low Ni(2+)- and amiloride-sensitive Ca2+ channels giving rise predominantly to I(T) can produce substantial amplification of synaptic input. We thus propose that these channels represent an important component of subthreshold signal integration in apical dendrites of CA1 pyramidal cells.