Neuroscience
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Stress alters memory. Understanding how and when acute stress improves or impairs memory is a challenge. Stressors can affect memory depending on a combination of factors. ⋯ To assess putative sources of the negative memory modulation effects induced during reconsolidation, current emotional state was evaluated immediately after Testing Session (day 7). An increase in arousal was revealed only when CPS was administered concurrently with memory reactivation-labilization. The possibility of integration during reconsolidation of independent associations of these emotive components in the trace is a critical factor in modulating neutral memories during reconsolidation by stressors.
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Previous experiences can drive adaptive behavior based on different characteristics, including contextual ones. Indeed, contextual information can be used as a criterion to guide the recall of the most relevant memory trace and the inhibition of others. The medial Prefontal Cortex (mPFC) has been proposed as an area that plays a pivotal role in regulating the retrieval of memory traces in downstream regions. ⋯ We also found an increase in c-Fos expression in the mPFC after mPFC 5-HT2aR blockade that does not correlate with the animals' behavioral response. However, these changes showed a significant correlation with those observed in the PRH. These results suggest that mPFC 5-HT2aR signaling may modulate the behavioral response during memory recall by controlling the neuronal activation in the PRH.
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Catecholaminergic transmission plays an essential role in both physiological and pathological cognitive functions. Plastic changes subserving learning and memory processes are highly dependent on catecholaminergic activity, altering their function and impacting cognition. This review assesses changes in the dopaminergic and norepinephrine systems as part of the mechanisms underlying cognitive impairment in Alzheimer's disease as associated with metabolic dysfunctions such as type 2 diabetes, metabolic syndrome, and neuroinflammation and peripheral inflammation. Understanding the role of catecholaminergic systems in these conditions is relevant for identifying etiological factors that could advance diagnostic and therapeutic approaches for ameliorating cognitive alterations, disease onset, and progression.
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Microglia are unique cells in the central nervous system (CNS), being considered a sub-type of CNS macrophage. These cells monitor nearby micro-regions, having roles that far exceed immunological and scavengering functions, being fundamental for developing, protecting and maintaining the integrity of grey and white matter. Microglia might become dysfunctional, causing abnormal CNS functioning early or late in the life of patients, leading to neurologic or psychiatric disorders and premature death in some patients. ⋯ Alzheimer Disease is the prototype of the neurodegenerative disorders associated with these TREM2 variants, named here the Microgliopathies Type II. Here, we review clinical, pathological and some molecular aspects of human diseases associated with primary microglia dysfunctions and briefly comment some possible therapeutic approaches to theses microgliopathies. We hope that our review might update the interesting discussion about the impact of intrinsic microglia dysfunctions in the genesis of some pathologic processes of the CNS.
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Episodic meal-related memories provide the brain with a powerful mechanism for tracking and controlling eating behavior because they contain a detailed record of recent energy intake that likely outlasts the physiological signals generated by feeding bouts. This review briefly summarizes evidence from human participants showing that episodic meal-related memory limits later eating behavior and then describes our research aimed at investigating whether hippocampal neurons mediate the inhibitory effects of meal-related memory on subsequent feeding. ⋯ I describe our evidence showing that ingestion activates the molecular processes necessary for synaptic plasticity and memory during the early postprandial period, when the memory of the meal would be undergoing consolidation, and then summarize our findings showing that neural activity in dHC neurons is critical during the early postprandial period for limiting future intake. Collectively, our evidence supports the hypothesis that dHC neurons mediate the inhibitory effects of ingestion-related memory on future intake and demonstrates that post-experience memory modulation is not confined to artificial laboratory memory tasks.