title: Ion channels generating complex spikes in cartwheel cells of the dorsal cochlear nucleus.
abstract: Cartwheel cells are glycinergic interneurons that modify somatosensory input to the dorsal cochlear nucleus. They are characterized by firing of mixtures of both simple and complex action potentials. To understand what ion channels determine the generation of these two types of spike waveforms, we recorded from cartwheel cells using the gramicidin perforated-patch technique in brain slices of mouse dorsal cochlear nucleus and applied channel-selective blockers. Complex spikes were distinguished by whether they arose directly from a negative membrane potential or later during a long depolarization. Ca(2+) channels and Ca(2+)-dependent K(+) channels were major determinants of complex spikes. Onset complex spikes required T-type and possibly R-type Ca(2+) channels and were shaped by BK and SK K(+) channels. Complex spikes arising later in a depolarization were dependent on P/Q- and L-type Ca(2+) channels as well as BK and SK channels. BK channels also contributed to fast repolarization of simple spikes. Simple spikes featured an afterdepolarization that is probably the trigger for complex spiking and is shaped by T/R-type Ca(2+) and SK channels. Fast spikes were dependent on Na(+) channels; a large persistent Na(+) current may provide a depolarizing drive for spontaneous activity in cartwheel cells. Thus the diverse electrical behavior of cartwheel cells is determined by the interaction of a wide variety of ion channels with a prominent role played by Ca(2+).
authors.affiliation: Oregon Hearing Research Center/ Vollum Institute, Mail Code L-335A, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA.
authors.forename: Yuil
authors.initials: Y
authors.lastname: Kim
authors.forename: Laurence O
authors.initials: LO
authors.lastname: Trussell
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D017626:Cochlear Nucleus / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D004594:Electrophysiology; D018682:GABA Agents / Q000494:pharmacology; D005998:Glycine / Q000502:physiology*; D018684:Glycine Agents / Q000494:pharmacology; D066298:In Vitro Techniques; D007395:Interneurons / Q000187:drug effects / Q000502:physiology*; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D008813:Mice, Inbred ICR; D018408:Patch-Clamp Techniques; D024681:Potassium Channels, Calcium-Activated / Q000187:drug effects / Q000502:physiology; D011689:Purkinje Cells / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D018682:GABA Agents; D018684:Glycine Agents; D007473:Ion Channels; D024681:Potassium Channels, Calcium-Activated; D015222:Sodium Channels; D002118:Calcium; D005998:Glycine