Dendritic sodium spikelets and low-threshold calcium spikes in turtle olfactory bulb granule cells.
Active dendritic membrane properties were investigated by whole cell recordings from adult turtle olfactory bulb granule cells. The laminar structure of the olfactory bulb allowed differential polarization of the distal apical dendrites versus the somatic part of the cells by an external electric field. Dendritic depolarization evoked small (approximately 10 mV) all-or-none depolarizing events of approximately 10-ms duration. These spikelets often occurred in bursts at high frequency (< or = 250 Hz); they were present despite the application of synaptic and gap junction antagonists, but were abolished by TTX and intracellularly applied QX314. The spikelets were interpreted as attenuated sodium spikes initiated in different branches of the granule cells dendrites. They occurred spontaneously, but could also be evoked by excitatory postsynaptic potentials (EPSPs) to the distal dendrites. Spikelets initiated by distal excitation could function as prepotentials for full sodium spikes, in part depending on the level of proximal depolarization. Somatic depolarization by the electric field evoked full sodium spikes as well as low-threshold calcium spikes (LTSs). Calcium imaging revealed that the electrophysiologically identified LTS evoked from the soma was associated with calcium transients in the proximal and the distal dendrites. Our data suggest that the LTS in the soma/proximal dendrites plays a major role in boosting excitability, thus contributing to the initiation of sodium spiking in this compartment. The results furthermore suggest that the LTS and the sodium spikes may act independently or cooperatively to regulate dendritic calcium influx.
Division of Neurophysiology, Department of Medical Physiology, University of Copenhagen, Copenhagen, Denmark.
Giulietta
G
Pinato
Jens
J
Midtgaard
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003712:Dendrites / Q000187:drug effects / Q000502:physiology*; D003952:Diagnostic Imaging / Q000379:methods; D004307:Dose-Response Relationship, Radiation; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D020748:Mibefradil / Q000494:pharmacology; D008959:Models, Neurological; D009474:Neurons / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D009532:Nickel / Q000494:pharmacology; D009830:Olfactory Bulb / Q000166:cytology* / Q000502:physiology; D018408:Patch-Clamp Techniques / Q000379:methods; D011724:Pyridazines / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014426:Turtles; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology
D002121:Calcium Channel Blockers; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D011724:Pyridazines; D020748:Mibefradil; D013779:Tetrodotoxin; C022838:nickel chloride; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; C056639:2-amino-5-phosphopentanoic acid; D009532:Nickel; C049853:gabazine; D012964:Sodium; D014633:Valine; D002118:Calcium