PMID- 12154177
OWN - NLM
STAT- MEDLINE
DCOM- 20030213
LR  - 20220309
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 542
IP  - Pt 3
DP  - 2002 Aug 1
TI  - Dendrotoxin-sensitive K(+) currents contribute to accommodation in murine spiral 
      ganglion neurons.
PG  - 763-78
AB  - 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.
FAU - Mo, Zun-Li
AU  - Mo ZL
AD  - Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 
      08854-8082, USA.
FAU - Adamson, Crista L
AU  - Adamson CL
FAU - Davis, Robin L
AU  - Davis RL
LA  - eng
GR  - NIDCD01856/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Elapid Venoms)
RN  - 0 (Kcna1 protein, mouse)
RN  - 0 (Neurotoxins)
RN  - 0 (Peptides)
RN  - 0 (Potassium Channels)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 119128-61-9 (dendrotoxin K)
RN  - 147173-20-4 (Kv1.1 Potassium Channel)
RN  - 74811-93-1 (dendrotoxin)
SB  - IM
MH  - Action Potentials/drug effects
MH  - Adaptation, Physiological/*physiology
MH  - Animals
MH  - Cells, Cultured
MH  - Elapid Venoms/*pharmacology
MH  - Electrophysiology
MH  - Kv1.1 Potassium Channel
MH  - Membrane Potentials/drug effects
MH  - Mice
MH  - Mice, Inbred CBA
MH  - Neurons/drug effects/*physiology
MH  - Neurotoxins/*pharmacology
MH  - Patch-Clamp Techniques
MH  - Peptides/pharmacology
MH  - Potassium Channels/drug effects
MH  - Potassium Channels, Voltage-Gated/*drug effects/*physiology
MH  - Spiral Ganglion/drug effects/*physiology
MH  - Time Factors
PMC - PMC2290456
EDAT- 2002/08/03 10:00
MHDA- 2003/02/14 04:00
PMCR- 2003/08/01
CRDT- 2002/08/03 10:00
PHST- 2002/08/03 10:00 [pubmed]
PHST- 2003/02/14 04:00 [medline]
PHST- 2002/08/03 10:00 [entrez]
PHST- 2003/08/01 00:00 [pmc-release]
AID - PHY_17202 [pii]
AID - 10.1113/jphysiol.2002.017202 [doi]
PST - ppublish
SO  - J Physiol. 2002 Aug 1;542(Pt 3):763-78. doi: 10.1113/jphysiol.2002.017202.