Figure 10

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 [34]. 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 GABA_BR which has been reported on the axon terminals of the ORNs [28] 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 GABA_BR). Therefore, we hypothesize that the GABA_BR 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 G_qα, and phospholipase Cβ in insect olfactory transduction [66]. Activation of GABA_BR 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 G_qα. In addition, our pharmacological results provide evidence that blocking the GABA_AR disturbs the Ca²⁺-response within the ORNs to a large degree. However, which neurons in the antennal lobes express the ionotropic GABA_AR has not yet been reported. Whether the GABA_AR-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 GABA_AR are speculative, and remain to be determined.