Abstract
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 Gα11 or Gαq produces equally well functioning signaling cascades, Gαq- and Gα11-deficient mice exhibit distinct alterations in motor coordination. By using whole-cell recordings and Ca2+ imaging in Purkinje cells, we show that Gαq is required for mGluR-dependent synaptic transmission and for long-term depression (LTD). Gα11 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 Gαq versus Gα 11. Our findings suggest an expression level-dependent action of Gαq and Gα11 for Purkinje cell signaling and assign specific roles of these two Gq isoforms for motor coordination.
Original language | English |
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Pages (from-to) | 5119-5130 |
Number of pages | 12 |
Journal | Journal of Neuroscience |
Volume | 24 |
Issue number | 22 |
DOIs | |
State | Published - 2 Jun 2004 |
Externally published | Yes |
Keywords
- Calcium [Ca] imaging
- G-protein
- Knock-out
- Motor control
- Patch clamp
- Purkinje cell
- RT-PCR
- Synaptic plasticity
- mGluR