Neuroscience
-
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.
-
Exposure to stressors in early postnatal life induces long-lasting modifications in brain function. This plasticity, an essential characteristic of the brain that enables adaptation to the environment, may also induce impairments in some psychophysiological functions, including learning and memory. Early life stress (ELS) has long-term effects on the hypothalamic-pituitary-adrenal axis response to stressors, and has been reported to lead to neuroinflammation, altered levels of neurotrophic factors, modifications in neurogenesis and synaptic plasticity, with changes in neurotransmitter systems and network functioning. ⋯ Studies are not always in agreement, however, no effects, or sometimes facilitation, being reported, depending on the nature and intensity of the early intervention, as well as the age when the outcome was evaluated and the sex of the animals. When considering processes occurring after consolidation, related with memory maintenance/persistence or transformation, there are a very reduced number of reports. Future studies addressing the mechanisms underlying memory changes for ELS should shed some light on the understanding of the different effects induced by stressors of different types and intensities on cognitive functions.
-
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.
-
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.
-
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.