Divorce of obligatory partners in pain: disruption of GABABreceptor heterodimers in neuralgia

It is now well established that G protein‐coupled receptors can exist not only as homodimers, but also as heterodimers or higher order oligomers. However, whether and how dimerization of the receptors is regulated is poorly understood. In this issue of The EMBO Journal , the team of Marc Landry provides evidence for an intriguing mechanism by which—under pathological conditions—GABA B receptor heterodimers at the cell surface are disrupted and thereby inactivated. An impressive set of experiments thus reveals a novel mechanism regulating the number of functional GABA B receptors in the plasma membrane and shows that the receptor heterodimer may not be as stable as we previously thought.