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Journal of Neuroscience, Vol 11, 2270-2280, Copyright © 1991 by Society for Neuroscience
The site for initiation of action potential discharge over the somatodendritic axis of rat hippocampal CA1 pyramidal neurons
RW Turner, DE Meyers, TL Richardson and JL Barker
Department of Physiology, University of British Columbia, Vancouver, Canada.
Early electrophysiological studies in the mammalian hippocampus reported
that orthodromic depolarization of pyramidal cells evoked action potential
discharge (presumed Na+ dependent) both at the axon hillock and at one or
more sites in the dendritic arborization (Cragg and Hamlyn, 1955; Andersen,
1959, 1960; Spencer and Kandel, 1961; Andersen and Lomo, 1966). Although
tetrodotoxin (TTX)-sensitive spikes have been recorded at the dendritic
level (Wong et al., 1979; Benardo et al., 1982; Miyakawa and Kato, 1986;
Turner et al., 1989), the site for initiation of these potentials has not
yet been determined. In this study, we examine the site for initiation of
Na+ spike discharge over the cell axis of rat hippocampal CA1 pyramidal
neurons. Intrasomatic and intradendritic recordings were obtained from
pyramidal neurons of hippocampal slices maintained in vitro. Spike
discharge was evoked by alvear (antidromic) stimulation or orthodromically
by stimulation of afferent inputs in stratum oriens (SO) or stratum
radiatum (SR). Antidromic and orthodromic spikes were greatest in amplitude
in somatic recordings and declined over the apical dendritic axis, while
spike half-width was shortest at the cell body and increased with distance
from stratum pyramidale. Measurements of orthodromic spike threshold
revealed that the only location at which spikes discharged at a consistent
membrane potential at threshold intensity (voltage threshold) was the cell
body region. Finally, at threshold intensity, SR-evoked intradendritic
spikes were blocked by local application of TTX in stratum pyramidale,
while spike blockade at suprathreshold intensity required the diffusion of
TTX into the apical dendritic region. These results indicate that, for
threshold intensities of stimulation, antidromic and orthodromic spike
discharge in CA1 pyramidal cells is initiated in the region of the cell
body layer, subsequently conducting over the apical dendrites in a
retrograde fashion. In contrast, SR-evoked orthodromic spike discharge
exhibits an intensity-dependent shift in the site of origin up to 200
microns within the apical dendritic arborization.
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