Neurobiology of learning and memory
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Neurobiol Learn Mem · Feb 2011
Editorial Biography Historical ArticleRF Thompson: a bridge between 20th and 21st century neuroscience.
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Neurobiol Learn Mem · Nov 2010
Angiotensin modulates long-term memory expression but not long-term memory storage in the crab Chasmagnathus.
Memory reconsolidation is a dynamic process in which a previously consolidated memory becomes labile following reactivation by a reminder. In a previous study in the crab Chasmagnathus memory model, we showed that a water-shortage episode, via angiotensin modulation during reconsolidation, could reveal a memory that otherwise remains unexpressed: weakly trained animals cannot reveal long-term memory (LTM) except when an episode of noticeable ethological meaning, water deprivation, is contingent upon reconsolidation. However, these results are at variance with two of our previous interpretations: weak training protocols do not build LTM and angiotensin II modulates the strength of the information storing process. ⋯ Results show that angiotensin modulates LTM expression but not LTM memory storage in the crab Chasmagnathus. The results lead us to suggest that, in Chasmagnathus, LTM expression - the process of gaining appreciable control over behavior of the reactivated trace in the retrieval session - may be considered a distinct attribute of its long-term storage. This strategy, a positive modulation during reconsolidation, is proposed to distinguish between memories that can be reactivated, labilized and are not expressed, and memories that are not stored long term, obliterated or altered in other retrieval mechanisms.
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Neurobiol Learn Mem · Nov 2010
Comparative StudyThe effects of midazolam and D-cycloserine on the release of glutamate and GABA in the basolateral amygdala of low and high anxiety rats during extinction trial of a conditioned fear test.
In this study, we investigated how midazolam and d-cycloserine regulate the tonic activity and/or phasic reactivity of brain neurotransmitter systems to fear-evoking stimuli in rats with varying intensities of a fear response. We used a new animal model composed of high (HR) and low (LR) anxiety rats, selected according to their behaviour in the contextual fear test (i.e., the duration of a freezing response was used as a discriminating variable). In these rats, we examined the effects of both drugs on the release of glutamate and GABA in the basolateral amygdala (BLA) during the first extinction trial of a conditioned fear test. ⋯ In HR animals, the pretreatment of rats with d-cycloserine and midazolam significantly increased the local concentration of GABA and inhibited the expression of contextual fear. These findings suggest that animals more vulnerable to stress have innate deficits in brain systems that control the activity of the BLA mediating the central effect of stress. These results contribute to our understanding of observed individual differences in the effects of anxiolytic drugs among patients with anxiety disorders.
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Neurobiol Learn Mem · Nov 2010
Sevoflurane impairs memory consolidation in rats, possibly through inhibiting phosphorylation of glycogen synthase kinase-3β in the hippocampus.
Sevoflurane administration impairs memory processes in both humans and animals. Increasing evidence suggests that enhancement of the phosphorylation state of glycogen synthase kinase-3β (GSK-3β), as a result of acute administration of lithium chloride (LiCl), may enhance memory consolidation. The current experiments examined whether GSK-3β phosphorylation was involved in mediating the memory impairing effects of posttraining sevoflurane on inhibitory avoidance (IA) retention. ⋯ In experiment 2, administration of LiCl (100mg/kg, intraperitoneally) 30 min before IA training not only blocked the sevoflurane-induced impairment of consolidation, but also reversed the inhibitory effect of sevoflurane on GSK-3β phosphorylation in the hippocampus. Collectively, these findings support the hypothesis that sevoflurane exposure can impair consolidation of IA memory in rats. Sevoflurane-induced amnesia may be due, at least in part, to suppression of GSK-3β phosphorylation in the hippocampus.
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Neurobiol Learn Mem · Oct 2010
Randomized Controlled TrialCortisol enhances neural differentiation during fear acquisition and extinction in contingency aware young women.
Previously, we observed cortisol induced enhancement of neural fear acquisition in women. Yet, less is known about cortisol effects on neural fear extinction. Via differential fear conditioning, we explored cortisol effects on acquisition and extinction. ⋯ During acquisition group differences were due to higher responses to the CS+ than to the CS- in the cortisol group. Notably, during extinction, group differences were due to higher responses to the CS- than to the CS+ in this group. Thus, cortisol induced a fear acquisition and extinction specific enhanced neural differentiation.