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The Journal of Neuroscience, June 2, 2004, 24(22):5119-5130; doi:10.1523/JNEUROSCI.4193-03.2004
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Cellular/Molecular
Distinct Roles of G q and G11 for Purkinje Cell Signaling and Motor Behavior
J. Hartmann,1
R. Blum,1
Y. Kovalchuk,1
H. Adelsberger,1
R. Kuner,2
G. M. Durand,1
M. Miyata,3
M. Kano,4
S. Offermanns,2 and
A. Konnerth1
1Institut für Physiologie, Ludwig-Maximilians-Universität, 80336 Munich, Germany, 2Institut für Pharmakologie, Universität Heidelberg, 69120 Heidelberg, Germany, 3National Institute for Physiological Sciences, Department of Information Physiology, Okazaki 444-8585, Japan, and 4Department of Cellular Neurophysiology, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8640, Japan
G-protein-coupled metabotropic glutamate group I receptors (mGluR1s) mediate synaptic transmission and plasticity in Purkinje cells and, therefore, critically determine cerebellar motor control and learning. Purkinje cells express two members of the G-protein Gq family, namely Gq and G11. Although in vitro coexpression of mGluR1 with either G 11 or Gq produces equally well functioning signaling cascades, Gq- and G11-deficient mice exhibit distinct alterations in motor coordination. By using whole-cell recordings and Ca2+ imaging in Purkinje cells, we show that Gq is required for mGluR-dependent synaptic transmission and for long-term depression (LTD). G11 has no detectable contribution for synaptic transmission but also contributes to LTD. Quantitative single-cell RT-PCR analyses in Purkinje cells demonstrate a more than 10-fold stronger expression of Gq versus G11. Our findings suggest an expression level-dependent action of Gq and G11 for Purkinje cell signaling and assign specific roles of these two Gq isoforms for motor coordination.
Key words: Purkinje cell; mGluR; G-protein; synaptic plasticity; motor control; patch clamp; calcium [Ca] imaging; knock-out; RT-PCR
Received Sep 12, 2003;
revised March 30, 2004;
accepted April 22, 2004.
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