Research interest
We are interested on synaptic transmission and plasticity and the role played by glutamate receptors. Our group provided the first evidence for the existence of kainate receptors (KARs) in the CNS (PNAS 1993), demonstrated that the 2, 3-benzodiazepine, GYKI53655, is a specific antagonist of AMPA receptors (Neuron 1995), making possible to study KARs in detail. Since then, we have proposed the existence of presynaptic KARs, which regulate the release of GABA (Neuron 1997), providing a rational basis to understand how KARs may participate in epilepsy. We found that KARs have a dual mechanism for signalling in that they are ion channels but also trigger a second messenger-mediated cascade which involves a G-protein activation (Neuron, 1998; P. N. A. S. 2000; Neuron, 2003). The finding that an ion channel-forming receptor is able to signal through a G-protein mediated metabotropic mechanism has opened new vistas on the operating mode of glutamate receptors of the ionotropic type (EMBO J., 2007; Neuron, 2009; J Neurosci, 2013).