Abstract

Glutamate and GABA are evolutionarily old neurotransmitters. While glutamate typically mediates excitatory currents, GABA typically is inhibitory. Strikingly, in recent years, we have learned that glutamate also binds to and activates ion channels of inhibitory families, whereas GABA binds to and activates ion channels of the glutamate receptor family. This symposium will highlight the molecular basis for these “mixed messages” and what they may mean for the function of nervous systems. The scientific purpose of the symposium is to introduce ion channel receptors with “the wrong” ligand: GABA-A receptors activated by glutamate, and ionotropic glutamate receptors (iGluRs) activated by GABA.

The three different speakers will tackle this topic from various angles and introduce different examples of such ion channels originating from different organisms. Stefan Gründer will introduce examples of ion channels from the cnidarian Nematostella belonging to the GABA-A receptor family that are activated by glutamate. Yuhong Wang will demonstrate that iGluRs have evolved into glycine receptors or GABA receptors (and vice versa) numerous times in different animals. Finally, Laetitia Mony will introduce mammalian iGluRs that signal after binding to GABA.

Long regarded as curiosities, it is time to consider that ion channel receptors with atypical ligands might not be so atypical, and that glutamate and GABA play important inhibitory and excitatory roles in nervous systems, respectively. The symposium will showcase examples from different organisms to also address the molecular basis behind the evolution of such function during the emergence of complex nervous systems.