Schematic diagram of a reciprocal synapse from the EPL of the olfactory bulb. Stimulation of mitral cells release glutamate, depolarizing granule cells (1) through VGCC and/or NMDA/AMPA receptors (2) increasing cytoplasmic Ca²⁺. (3). This depolarization of granule cells induces exocytosis of GABA. On the other hand, the increase of intracellular Ca²⁺ or/and the activation of mGlu receptors (2-3) triggers the synthesis of endocannabinoids (anandamide/2AG) (4) which diffuse to the extracellular space (5) activating cannabinoid CB receptors (6) at the level of the granule cells and possible also the mitral cells terminals. This activation of CB receptors is able to inhibit GABA release (and eventually Glu release?). The eCB transporter (7) and the catabolic enzymes eliminate eCBs (8). Acute stress is apparently able to induce synthesis of eCB (4) and inhibit GABA release; this effect can be potentiated when the eCBs transporter (7) or the catabolizing enzyme (8) is blocked or when the synthesis of 2AG is inhibited with THL. NMDA/AMPA: inotropic glutamate receptors, mGluR: Metabotropic glutamate receptor, VGCC: Voltage-gated Ca²⁺ channels, AEAT: Arachidonyl ethanol amine transporter, CBR: Cannabinoid receptor, FAAH: Fatty acid amide hydrolase, GABA: γ-amino butyric acid, eCB: endocannabinoid, 2AG: 2-arachidonylglicerol, THL: tetrahydrolipostatin. *Modulator sites of acute immobilization stress.