T. Gillessen et C. Alzheimer, AMPLIFICATION OF EPSPS BY LOW NI2-SENSITIVE AND AMILORIDE-SENSITIVE CA2+ CHANNELS IN APICAL DENDRITES OF RAT CA1 PYRAMIDAL NEURONS(), Journal of neurophysiology, 77(3), 1997, pp. 1639-1643
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 excitat
ory 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 combine
d with local application of antagonists of I-T. Dendritic application
of low concentrations of Ni2+ (5 mu M) and amiloride (50 mu M) reduced
EPSP amplitude measured at the soma (resting membrane potential -70 m
V) 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 IT activation, the inhibito
ry 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 produ
ced only weak reduction of EPSP amplitude. Our data indicate that dend
ritic low Ni2+- and amiloride-sensitive Ca2+ channels giving rise pred
ominantly to I-T can produce substantial amplification of synaptic inp
ut. We thus propose that these channels represent an important compone
nt of subthreshold signal integration in apical dendrites of CA1 pyram
idal cells.