Dendrotoxin-sensitive K(+) currents contribute to accommodation in murine spiral ganglion neurons.
We have previously identified two broad electrophysiological classes of spiral ganglion neuron that differ in their rate of accommodation (Mo & Davis, 1997a). In order to understand the underlying ionic basis of these characteristic firing patterns, we used alpha-dendrotoxin (alpha-DTX) to eliminate the contribution of a class of voltage-gated K(+) channels and assessed its effects on a variety of electrophysiological properties by using the whole-cell configuration of the patch-clamp technique. Exposure to alpha-DTX caused neurons that initially displayed rapid accommodation to fire continuously during 240 ms depolarizing test pulses within a restricted voltage range. We found a non-monotonic relationship between number of action potentials fired and membrane potential in the presence of alpha-DTX that peaked at voltages between -40 to -10 mV and declined at more depolarized and hyperpolarized test potentials. The alpha-DTX-sensitive current had two components that activated in different voltage ranges. Analysis of recordings made from acutely isolated neurons gave estimated half-maximal activation voltages of -63 and 12 mV for the two components. Because alpha-DTX blocks the Kv1.1, Kv1.2 and Kv1.6 subunits, we examined the action of the Kv1.1-selective blocker dendrotoxin K (DTX-K). We found that this antagonist reproduced the effects of alpha-DTX on neuronal firing, and that the DTX-K-sensitive current also had two separate components. These data suggest that the transformation from a rapidly adapting to a slowly adapting firing pattern was mediated by the low voltage-activated component of DTX-sensitive current with a potential contribution from the high voltage-activated component at more depolarized potentials. In addition, the effects of DTX-K indicate that Kv1.1 subunits are important constituents of the underlying voltage-gated potassium channels.
Mo
Zun-Li
ZL
Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854-8082, USA.
Adamson
Crista L
CL
Davis
Robin L
RL
D000200:Action Potentials / Q000187:drug effects; D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D002478:Cells, Cultured; D004546:Elapid Venoms / Q000494:pharmacology*; D004594:Electrophysiology; D051662:Kv1.1 Potassium Channel; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008808:Mice, Inbred CBA; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009498:Neurotoxins / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects* / Q000502:physiology*; D013136:Spiral Ganglion / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors
D004546:Elapid Venoms; C496947:Kcna1 protein, mouse; D009498:Neurotoxins; D010455:Peptides; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; C081506:dendrotoxin K; D051662:Kv1.1 Potassium Channel; C020273:dendrotoxin