Schematic model of synaptic interactions within the antennal lobes. Spikes (action potentials) triggered by odors in ORNs propagate to the axon terminals, where they activate the VGCCs yielding to Ca2+-influx that serves as an intracellular signal to release the neurotransmitter (acetylcholine: Ach). This Ca2+-entry may also trigger Calcium-Induced Calcium-Release (CICR) through the ryanodine receptor (RyR) located in the endoplasmic reticulum (ER), amplifying the Ca2+-transient . Subsequently, the released-Ach activates the AchR located on the post-synaptic neurons (projection neurons: PNs). Released-Ach might also activate (directly or indirectly) the GABAergic local interneurons (LNs) (in a manner that remains to be precisely determined), in-turn, releasing the GABA that may act on the presynaptic ORN terminals via the GABA receptors. Metabotropic GABABR which has been reported on the axon terminals of the ORNs  may activate certain G-proteins (not yet precisely characterized in the ORNs), which for a relatively long odor application, such as 5 s (as in this study) might trigger the second component of the Ca2+ -response by activating directly or indirectly the InsP3R (since blocking the G-proteins by the pertussis-toxin yields a similar effect to blocking directly the GABABR). Therefore, we hypothesize that the GABABR activated G-proteins might activate (directly or putatively indirectly through membrane channels) a phospholipase C (PLC) to catalyze the synthesis of diacylglycerol and InsP3 from PIP2 (phospho-inositol bis-phosphate). Interestingly, a former study has described a role for Gqα, and phospholipase Cβ in insect olfactory transduction . Activation of GABABR in the ORN terminals might lead to InsP3-mediated Ca2+ -release from the ER that could in turn also trigger CICR through RyR as a putative second step to amplify or maintain the Ca2+ -transient. Some components of this pathway still remain to be investigated, such as the putative phospholipase C, as well as the different isoforms of G-proteins, and notably the Gqα. In addition, our pharmacological results provide evidence that blocking the GABAAR disturbs the Ca2+-response within the ORNs to a large degree. However, which neurons in the antennal lobes express the ionotropic GABAAR has not yet been reported. Whether the GABAAR-effect occurs directly or indirectly on the ORNs remains to be investigated. Note that in this model the localization of the AchR (both muscarinic and nicotinic) and GABAAR are speculative, and remain to be determined.