In summary, we demonstrate in this study that alternative splicing of the mouse Girk2 gene generates at least two variants, and that these splice variants can give rise to channel subtypes that differ in terms of their subcellular trafficking and the neurophysiological processes in which they participate. As GIRK-dependent signaling plays an important role in moderating glutamatergic input to neurons, our findings raise the intriguing possibility that altering the balance of GIRK2 splice variants could represent a means by which neurons fine-tune the processing of excitatory synaptic input, in a subcellular compartment-dependent manner.
