GABAergic interneurons are known to inhibit 5-HT neuronal activity via GABA-A receptors (1). Because of 5-HT release during stress, 5-HT2C receptors expressed by GABAergic interneurons are activated (2), which leads to a GABA-mediated negative feedback control of 5-HT neuron during stress (Mongeau et al., 2010). Glutamatergic (Glu) projections from forebrain (cortex) areas also excite GABAergic interneurons (3), but inhibitory terminal GABA-B1a subunit containing heteroreceptors exert a presynaptic modulation on these projections (4). Accordingly, the excitatory influence of cortical glutamatergic projections onto GABA interneurons is larger in GABA-B1a−/− mice, which would account for a reduced 5-HT turnover in these mutants.