Figure 5. Schematic illustration of the effect of different brain areas and various neurotransmitter mechanisms in the modulation of state-dependent memory induced by morphine. Some documents reported that opioidergic (Jafari-Sabet and Jannat-Dastjerdi, 2009), muscarinic cholinergic (Jafari-Sabet, 2011), and α2-adrenergic (Jafari-Sabet et al., 2013), systems in the CA1 area are essential for inducing muscimol-related state-dependent memory (Jafari-Sabet et al., 2014). Moreover, cholinergic and serotonergic receptor systems of the CeA play a key role in morphine-induced state-dependent memory (Tirgar et al., 2014). In the medial septum, there is cross state-dependent memory retrieval between cannabinoid and acetylcholine or ethanol (Alijanpour and Rezayof, 2013). Also, cholinergic and glutamatergic receptors of the VTA participate in morphine state-dependent learning (Ahmadi et al., 2007). Also, nitric oxide, cholinergic and dopaminergic systems, of the NAc are involved in morphine state-dependent learning (Zarrindast et al., 2012b). CeA: central nucleus of the amygdala, VTA: ventral tegmental area, and NAc: nucleus accumbens.