The transient receptor potential (TRPC) proteins
form non-selective cation channels that are activated downstream
of Gq-phospholipase C-coupled receptors. TRPC3,
one of the seven members of the TRPC subfamily, combines
functions of an unspecific ion channel and a signal transducer.
In the mammalian brain, the expression of TRPC3 is highest
in cerebellar Purkinje cells, the principal neurons, and the sole
output of the cerebellar cortex. In this review, we summarize
findings identifying TRPC3 channels as integral components
of glutamatergic metabotropic synaptic transmission.We give
an overview of postsynaptic interaction partners and activation
mechanisms of TRPC3 in central neurons. Finally, we
address the deleterious consequences of distorted TRPC3 synaptic
signaling for cerebellar function in different mouse
models and present TRPC3 as an emerging candidate protein
implicated in various forms of ataxia in humans.