Initiation and propagation of regenerative Ca(2+)-dependent potentials in dendrites of layer 5 pyramidal neurons.
The initiation and propagation of dendritic Ca(2+)-dependent regenerative potentials (CDRPs) were investigated by imaging the Ca(2+)-sensitive dye Fluo-4 during whole cell recording from the soma of layer 5 pyramidal neurons visualized in a slice preparation of rat neocortex by the use of infrared-differential interference contrast microscopy. CDRPs were evoked by focal iontophoresis of glutamate at visually identified sites 178-648 microm from the soma on the apical dendrite and at sites on the basal dendrites. Increases in [Ca(2+)](i) were maximal near the site of iontophoresis and were graded with iontophoretic current that was subthreshold for evoking CDRPs. CDRP initiation was associated with a [Ca(2+)](i) rise that differed from a just-subthreshold response in both magnitude and spatial extent but whose amplitude declined both proximal and distal to the iontophoretic site. These [Ca(2+)](i) rises, whether associated with subthreshold or regenerative voltage responses, were minimally affected by blockade of N-methyl-D-aspartate receptors but were abolished by Cd(2+), suggesting that Ca(2+) influx through voltage-gated channels caused the rise of [Ca(2+)](i). On the assumption that the rise of [Ca(2+)](i) during a CDRP marks the spatial extent of regenerative Ca(2+) influx, we conclude that CDRPs can be evoked at any point on the main apical or basal trunk where membrane potential reaches CDRP threshold rather than at discrete "hot spots," the CDRP is initiated at a spatially restricted site, and it propagates decrementally both distal and proximal to its initiation site. These results raise the possibility that synaptic integration may occur first in the dendrites to evoke a CDRP. Because these responses propagate decrementally to the soma, they are able to sum with input from other regions of the cell so that the cell as a whole remains integrative.
Oakley
J C
JC
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195-7290, USA.
Schwindt
P C
PC
Crill
W E
WE
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000814:Aniline Compounds; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology; D003712:Dendrites / Q000378:metabolism*; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D005456:Fluorescent Dyes; D018698:Glutamic Acid / Q000494:pharmacology; D015640:Ion Channel Gating / Q000502:physiology; D007478:Iontophoresis; D008297:Male; D008856:Microscopy, Fluorescence; D019579:Neocortex / Q000166:cytology; D009924:Organ Culture Techniques; D017966:Pyramidal Cells / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D013268:Stimulation, Chemical; D014966:Xanthenes
D000814:Aniline Compounds; D015220:Calcium Channels; C409648:Fluo 4; D005456:Fluorescent Dyes; D014966:Xanthenes; D002104:Cadmium; D018698:Glutamic Acid; D002118:Calcium