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Significance We established a new genetic method for rapidly activating Cre recombinase that is based on suppression of a nonsense codon within Cre by a new generation of aminoglycosides. We applied this strategy to successfully silence both enzymes responsible for GABA biosynthesis in hypothalamic agouti-related peptide (AgRP) neurons that control appetite and other behaviors. Inactivation of GABA signaling in AgRP neurons of young adult mice resulted in severe loss of body weight and abnormal glucose metabolism, whereas older mice only manifested transient appetite deficiency. This genetic system adds another robust tool that can be used to understand complex neurological processes.

New inducible genetic method reveals critical roles of GABA in the control of feeding and metabolism