The metabotropic glutamate receptor subtype 1 (mGluR1) is abundantly expressed at parallel fiber (PF)-Purkinje cell (PC) synapses and is crucial for cerebellar function. Stimulation of mGluR1 at PF-PC synapses is followed by two G-proteindependent processes: production of IP₃ leading to Ca²⁺ release from intracellular stores and initiation of a slowly activating EPSC (I_mGluR ). It was previously reported that I_mGluR is mediated by the cation channel TRPC1 (Kim et al., Nature, 2003). TRPC1 is able to form heteromeric channel complexes with TRPC4 and TRPC5 of which only TRPC4 is expressed in mouse PCs (s. poster by Dragicevic et al.). We studied mGluR-dependent synaptic transmission in mice deficient for TRPC1 and TRPC4 by using whole-cell recordings and Ca²⁺ imaging in acute cerebellar slices. Strikingly, we found that repetitive PF stimulation evokes I_mGluR in these mutant mice. Moreover, the mGluR1-agonist DHPG when pressure-ejected to dendrites of PCs is able to activate I_mGluR in the absence of TRPC1 and TRPC4. The amplitudes of current and Ca²⁺ responses in both cases were not significantly different from those recorded in control mice. Thus, neither TRPC1 nor TRPC4 render a major contribution to mGluR-dependent synaptic transmission at the PFPC synapse.