Neuroscience
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Oxytocin (OT) and vasopressin (AVP) are two closely related neuropeptides implicated in learning and memory processes, anxiety, nociception, addiction, feeding behavior and social information processing. Regarding learning and memory, OT has induced long-lasting impairment in different behaviors, while the opposite was observed with AVP. We have previously evaluated the effect of peripheral administration of OT or its antagonist (AOT) on the inhibitory avoidance response of mice and on the modulation of cholinergic mechanisms. ⋯ Administration of anticholinesterases inhibitors with access to the central nervous system (CNS), the activation of muscarinic acetylcholine (Ach) receptors and the increase of evoked ACh release using linopirdine (Lino) (3-10 µg/kg, IP), reversed the impairment of retention performance induced by OT. Besides, either muscarinic or nicotinic antagonists with unrestricted access to the CNS reduced the magnitude of the performance-facilitating effect of AOT's central infusion. We suggest that OT might induce a cholinergic hypofunction state, resulting in an impairment of IA memory formation, a process for which the cholinergic system is crucially necessary.
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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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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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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.
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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.