Neuroscience
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The present paper provides a comprehensive review of latent extinction. In maze learning situations, latent extinction involves confining an animal to a previously reinforced goal location without food. When returned to the starting position after latent extinction, the animal typically shows a response decrement. ⋯ The hippocampus is critically involved in latent extinction, whereas other brain regions typically implicated in regular "response extinction" in the maze, such as the dorsolateral striatum, are not required for latent extinction. Similar to other kinds of learning, latent extinction requires NMDA receptor activity, suggesting the involvement of synaptic plasticity. Consistent with a multiple memory systems perspective, research on latent extinction supports the hypothesis that extinction learning is not a unitary process but rather there are different kinds of extinction learning mediated by distinct neural systems.
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The amygdala, specifically its basolateral nucleus (BLA), is a critical site integrating neuromodulatory influences on memory consolidation in other brain areas. Almost 20 years ago, we reported the first direct evidence that BLA activity is required for modulatory interventions in the entorhinal cortex (EC) to affect memory consolidation (Roesler, Roozendaal, and McGaugh, 2002). Since then, significant advances have been made in our understanding of how the EC participates in memory. ⋯ The findings suggest that the EC may function as a gateway and mediator of modulatory influences from the BLA, which are then processed and relayed to the HIP. Through extensive reciprocal connections among the EC, HIP, and several cortical areas, information related to new memories is then consolidated by these multiple brain systems, through various molecular and cellular mechanisms acting in a distributed and highly concerted manner, during several hours after learning. A special note is made on the contribution by Ivan Izquierdo to our understanding of memory consolidation at the brain system level.
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A possible role for the brain β-endorphin system in memory modulation was proposed by Ivan Izquierdo more than 30 years ago. Along with pharmacologic evidence of the effects of morphine and naloxone administered immediately after training in avoidance tasks and with the demonstration of medial-basal hypothalamus β-endorphin release after novelty detection, it was hypothesized that an endogenous opioid state present in the labile period of consolidation will be part of the memory of the newly acquired information. ⋯ In this review some of the original papers in the subject are revisited. Recent studies on the memory beneficial effects of novelty, both in animal models and in humans, indicate this is line of investigation is worth of pursuing and demonstrate the importance of the seminal work of Ivan Izquierdo in the field of memory modulation.
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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.