 |
 Previous Article | Next Article 
The Journal of Neuroscience, April 15, 1999, 19(8):2852-2864
Specific Alteration of Spontaneous GABAergic Inhibition in
Cerebellar Purkinje Cells in Mice Lacking the Potassium Channel
Kv1.1
Chuan-Li
Zhang1,
Albee
Messing2, and
Shing Yan
Chiu1
1 Department of Physiology, University of Wisconsin
School of Medicine, Madison, Wisconsin 53706, and
2 Department of Pathobiological Sciences, School of
Veterinary Medicine, and Waisman Center, University of Wisconsin,
Madison, Wisconsin 53705
In the cerebellum, the basket cell innervation on Purkinje cells
provides a major GABAergic inhibitory control of the single efferent
output from the cerebellum. The Shaker-type K channel Kv1.1 is
localized at the axon arborization preceding the terminal of the basket
cells and is therefore a potential candidate for regulating the
GABAergic inhibition. In this study, we directly assess this role of
Kv1.1 by electrophysiological analysis of Kv1.1 null mutant mice.
Whole-cell patch-clamp recordings of spontaneous IPSCs (sIPSCs)
were made from Purkinje cells in thin cerebellar slices from postnatal
day (P)10-15 Kv1.1-null mutants using wild-type littermates as
controls. The null mutation confers a very specific change in the
sIPSC: the frequency increases about twofold, without accompanying
changes in the mean and variance of its amplitude distribution. The
frequency and amplitude of the miniature IPSCs (mIPSCs) are unaffected.
Spontaneous firing rate of the basket cells is unaltered. Evoked IPSC
does not show multiple activity in the mutants. Motor skills tests show
that Kv1.1 null mice display a compromised ability to maintain balance
on a thin stationary rod. We conclude that the Kv1.1 null mutation
results in a persistent elevation of the tonic inhibitory tone on the
cerebellum Purkinje cell efferent and that this is not fully
compensated for by residual Shaker-type channels. We further suggest
that the increase in inhibitory tone in the mutants might underlie the
behavioral deficits. At the cellular level, we propose that Kv1.1
deletion enhances excitability of the basket cells by selectively
enhancing the likelihood of action potential propagation past axonal
branch points.
Key words:
potassium channel gene; homologous recombination; cerebellum; GABA; mouse; Purkinje cell
Copyright © 1999 Society for Neuroscience 0270-6474/99/1982852-13$05.00/0
This article has been cited by other articles:
|
|
|
|
 
H. M. Brew, J. X. Gittelman, R. S. Silverstein, T. D. Hanks, V. P. Demas, L. C. Robinson, C. A. Robbins, J. McKee-Johnson, S. Y. Chiu, A. Messing, et al.
Seizures and Reduced Life Span in Mice Lacking the Potassium Channel Subunit Kv1.2, but Hypoexcitability and Enlarged Kv1 Currents in Auditory Neurons
J Neurophysiol,
September 1, 2007;
98(3):
1501 - 1525.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. E. Metz, N. Spruston, and M. Martina
Dendritic D-type potassium currents inhibit the spike afterdepolarization in rat hippocampal CA1 pyramidal neurons
J. Physiol.,
May 15, 2007;
581(1):
175 - 187.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Khavandgar, J. T. Walter, K. Sageser, and K. Khodakhah
Kv1 channels selectively prevent dendritic hyperexcitability in rat Purkinje cells
J. Physiol.,
December 1, 2005;
569(2):
545 - 557.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Chen, W. Gao, K. C. Reinert, L. S. Popa, C. M. Hendrix, M. E. Ross, and T. J. Ebner
Involvement of Kv1 Potassium Channels in Spreading Acidification and Depression in the Cerebellar Cortex
J Neurophysiol,
August 1, 2005;
94(2):
1287 - 1298.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. D. Kline, M. C. F. Buniel, P. Glazebrook, Y.-J. Peng, A. Ramirez-Navarro, N. R. Prabhakar, and D. L. Kunze
Kv1.1 Deletion Augments the Afferent Hypoxic Chemosensory Pathway and Respiration
J. Neurosci.,
March 30, 2005;
25(13):
3389 - 3399.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Kopp-Scheinpflug, K. Fuchs, W. R. Lippe, B. L. Tempel, and R. Rubsamen
Decreased Temporal Precision of Auditory Signaling in Kcna1-Null Mice: An Electrophysiological Study In Vivo
J. Neurosci.,
October 8, 2003;
23(27):
9199 - 9207.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. D Dodson, B. Billups, Z. Rusznak, G. Szucs, M. C Barker, and I. D Forsythe
Presynaptic rat Kv1.2 channels suppress synaptic terminal hyperexcitability following action potential invasion
J. Physiol.,
July 1, 2003;
550(1):
27 - 33.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Yuan and W. D Atchison
Methylmercury differentially affects GABAA receptor-mediated spontaneous IPSCs in Purkinje and granule cells of rat cerebellar slices
J. Physiol.,
July 1, 2003;
550(1):
191 - 204.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. M Brew, J. L Hallows, and B. L Tempel
Hyperexcitability and reduced low threshold potassium currents in auditory neurons of mice lacking the channel subunit Kv1.1
J. Physiol.,
April 1, 2003;
548(1):
1 - 20.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. J. Ebner and G. Chen
Spreading Acidification and Depression in the Cerebellar Cortex
Neuroscientist,
February 1, 2003;
9(1):
37 - 45.
[Abstract]
[PDF]
|
|
|
|
|
|
|
B. Maylie, E. Bissonnette, M. Virk, J. P. Adelman, and J. G. Maylie
Episodic Ataxia Type 1 Mutations in the Human Kv1.1 Potassium Channel Alter hKvbeta 1-Induced N-Type Inactivation
J. Neurosci.,
June 15, 2002;
22(12):
4786 - 4793.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. M. Kullmann, R. Rea, A. Spauschus, and A. Jouvenceau
The Inherited Episodic Ataxias: How Well Do We Understand the Disease Mechanisms?
Neuroscientist,
February 1, 2001;
7(1):
80 - 88.
[Abstract]
[PDF]
|
|
|
|
|
|
|
L. Zhou, A. Messing, and S. Y. Chiu
Determinants of Excitability at Transition Zones in Kv1.1-Deficient Myelinated Nerves
J. Neurosci.,
July 15, 1999;
19(14):
5768 - 5781.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
