Neuroscience
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For decades, Izquierdo and colleagues contributed to building the notion that declarative memory requires different processes at the molecular and systems levels. This review aims to discuss part of Izquierdo's legacy, mainly but not exclusively that related to fear memory. ⋯ Then, the underlying processes of declarative memory are depicted, discussing the formation, the nature and the progression of the memory trace in short-term and long-term memory, and describing the involvement of some molecular cascades in the hippocampal formation, mesocortex and frontal areas. Potential contributions to therapy or understanding cognitive processes are mentioned.
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Anxiety disorders are the most frequent type of mental disorder. Threat-conditioning memory plays a central role in anxiety disorders, impacting complex cognitive systems by modifying behavioral responses to fearful stimuli and inducing an overestimation of potential threats. Here, we analyzed the reminder-dependent amnesia on physiological responses, unconditioned stimulus (US) expectancy ratings, and measures of cognitive bias towards the threat of a threat-conditioning memory. ⋯ Tasks targeting stimulus representation, valuation, and attentional bias towards threat were performed. We show that the reminder-dependent intervention with an HWM weakened memory retention as expressed in skin conductance response (SCR) and faded the representation and valuation towards the threat, but it did not affect US expectancy or attentional bias. Our findings provide evidence for the experimental psychopathology approach opening the possibility to weaken both Threat conditioning memory and the systems associated with the maintenance of anxiety features.
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Recognizing and weighing the value of stimuli is necessary for survival, as it allows living things to respond quickly and adequately to new experiences by comparing them with previous ones. Recent evidence shows that context change could affect flavor learning, suggesting a more intricate scenario during complex associations of stimuli with opposite or different valence in a motivational conflict task. Furthermore, linked to the ability to weigh the value of stimuli is the ability to predict the consequences associated with them from previous experiences. ⋯ NMDARs activation in the IC decreases avoidance memory formation during a complex task (MIA) but not memory formation for an appetitive context. Furthermore, NMDARs activation does not affect the transition from appetitive to aversive learning. Overall, our results propose a different IC-NMDARs function during novel learning and memory updating.
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In marked contrast to the ample literature showing that the dorsal striatum is engaged in memory consolidation, little is known about its involvement in memory retrieval. Recent findings demonstrated significant increments in dendritic spine density and mushroom spine counts in dorsal striatum after memory consolidation of moderate inhibitory avoidance (IA) training; further increments were found after strong training. ⋯ Similar changes in mushroom and thin spine populations were found in the ventral striatum (nucleus accumbens), but they were related to the aversive stimulation and not to memory retrieval. These results suggest that memory retrieval is a dynamic process which produces neuronal structural plasticity that might be necessary for maintaining or strengthening assemblies that encode stored information.
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The endocannabinoid system is involved in the fine-tuning of local synaptic plasticity in the hippocampus during the initial steps of memory formation/transformation. In spite of extensive studies, endocannabinoid modulation of these processes is still poorly understood. Here we studied the effects of intra-CA1 infused AM404, an anandamide (AEA) transport/metabolism inhibitor, upon an aversive memory consolidation with or without prior systemic administration of metyrapone, as well the concomitant intra-CA1 administration of AM404 plus AM251 (CB1 receptor inverse-agonist), capsazepine (TRPV1 receptor antagonist) or tropicamide (M4 receptor antagonist). ⋯ This confirms that CB1 actually mediate the amnestic effect caused by the augmented AEA pool, but TRPV1 does not. The tropicamide result suggests an interesting comodulatory interaction between the endocannabinoid and the cholinergic systems. We propose a steady-state model centered in the idea of an optimal, stable extracellular concentration of anandamide as a necessary condition to ensure the consolidation of a stable memory trace in the CA1 area.