State-dependent memory and its modulation by different brain areas and neurotransmitters

Abstract

The state-dependent memory defines as a state that the retrieval of recently obtained information may be potential if the subject exists in a similar physiological situation as for the period of the encoding stage. Studies revealed that exogenous and endogenous compounds could induce state-dependent memory. The state-dependent memory made it probable to differentiate the effects of drugs per se on learning from the effects due to alterations in drug state during the task. Studies proposed the role of regions beyond the limbic formation and illustrated that state-dependent memory produced by various neurotransmitter systems and pharmacological compounds. Our review of the literature revealed that: (a) re-administration of drugs on the same state induce state-dependent memory; (b) many neurotransmitters induce endogenous state-dependent memory; (c) there are cross state-dependent learning and memory between some drugs; (d) some sites of the brain including the CA1 areas of the hippocampus, central nucleus of the amygdala (CeA), septum, ventral tegmental area (VTA), and nucleus accumbens (NAC) are involved in state-dependent memory. See also Figure 1(Fig. 1).

Keywords: CA1; CeA; neurotransmitter; pharmacological compounds; state-dependent memory.

Table 1. Effect of various neurotransmitters and pharmacological compounds on state-dependent memory produced by morphine

Table 2. Effect of some neurotransmitters on state-dependent memory elicited by ethanol

Table 3. Effect of some neurotransmitters and pharmacological compounds on state-dependent memory induced by acetylcholine

Figure 1. Graphical abstract

Figure 2. Schematic diagram of the influence of different neurotransmitters on the state-dependent memory produced by morphine. Morphine state-dependent learning could be affected by the cholinergic (Jafari et al., 2006), GABAergic (Zarrindast et al., 2006e), dopaminergic (Zarrindast et al., 2006b), histaminergic (Zarrindast et al., 2006d), glutamatergic (Zarrindast et al., 2014), and adrenergic systems (Khavandgar et al., 2002). These neurotransmitters modify morphine state-dependent memory.

Figure 3. Schematic model of ethanol-induced state-dependent memory. Ethanol activates GABA_A receptors which conduct Cl^-, resulting in neuronal hyperpolarization. Furthermore, PKC has a modulatory effect in the response of the GABA_A receptor to ethanol. Also, ethanol influences NMDA receptors which lead to inhibition of EPSP which decreased LTP. It is possible that ethanol causes storage deficiency in the training day and does not affect retrieval in the testing day hence producing a state-dependent memory (Miller et al., 1978).

Figure 4. Schematic model of possible pathways for state-dependent memory in the brain. The hippocampus, septum, amygdala, VTA, NAc, and cortex form a complex network of brain systems for modulation of state-dependent memory (Jafari-Sabet and Jannat-Dastjerdi, 2009)

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