Glucocorticoids act on glutamatergic pathways to affect memory processes

Sandi, Carmen

doi:10.1016/j.tins.2011.01.006

Cited by 148 publications

(130 citation statements)

References 101 publications

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“…This condition is optimal for hippocampal function. At high levels of cortisol the GRs begin to saturate and hippocampal performance deteriorates, with gradual deactivation of neural activity (Joëls & de Kloet, 1990, 1991Joëls, 2006;Sandi, 2011). Effects of GR activation are not immediate.…”

Section: Effects Of Stress On Memory-related Brain Regionsmentioning

confidence: 99%

Effects of psychosocial stress on episodic memory updating

et al. 2013

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Section: Effects Of Stress On Memory-related Brain Regionsmentioning

confidence: 99%

Effects of psychosocial stress on episodic memory updating

et al. 2013

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“…Glucocorticoids and the noradrenergic system have been identified as key mediators of the cognitive effects of stress [1,2,9,10]. Adrenal glucocorticoids, steroid hormones produced by the adrenal glands, can cross the blood-brain barrier, gaining access to the brain.…”

Section: Stress Mediators: Glucocorticoids and Norepinephrinementioning

confidence: 99%

“…In particular, a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) trafficking has been highlighted among the mechanisms whereby stress and glucocorticoids facilitate spatial memory [22 ] and LTP [23]. Recent findings have implicated the mechanisms that underlie LTD induction among those that mediate the impairing effects of stress and glucocorticoids in the retrieval of information [24], including the activation of extrasynaptic GluN2B subunit-containing Nmethyl-D-aspartate receptors (NMDARs) and the endocytosis of the GluA2 AMPAR subunit [9,24]. Regarding other synaptic proteins, strong evidence has accumulated for the involvement of the neural cell adhesion molecules (NCAM) in both facilitating [25] and impairing [26] effects of stress in memory function [27].…”

mentioning

confidence: 99%

Neural mechanisms and computations underlying stress effects on learning and memory

Luksys

Sandi

2011

Current Opinion in Neurobiology

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Stress has complex effects on memory function that can vary depending on the type of information that is learned and in relation to inter-individual characteristics. Recent work has also shown that stress can switch performance between memory systems, biasing it toward habit in detriment of spatial or goaldirected strategies. In addition, novel synaptic mechanisms have been implicated in the effects of stress in plasticity and memory. Computational modeling is emerging as a useful approach to integrate and to ascertain neural and cognitive computations underlying different effects of stress in memory. Having provided novel explanations for the inverted-U-shaped relationship between stress and cognitive performance, modelbased analysis studies can improve our understanding of diverse effects of stress in cognition and psychopathology. IntroductionStress can have profound effects on memory function, both when chronically experienced and when acutely coupled with a cognitive challenge [1]. In this review, we mainly focus on the effects of acute stress on learning, memory, and underlying mechanisms. We will also examine new modeling approaches aiming to ascertain the neural computations that underlie stress effects in these cognitive processes.It is generally accepted that acute stress or elevated stress hormones facilitate memory consolidation while impairing the retrieval of information [2]. Moreover, acute stress is generally highly disruptive for working memory processing, while it can facilitate implicit learning [1,2,3 ]. Recently, several animal and human studies showed that stress switches performance between memory systems, promoting a transition from 'flexible' spatial or goaldirected learning to 'rigid' habitual stimulus-response (S-R) cognitive strategies [4 ,5 ,6,7].However, one should be cautious when summarizing the effects of stress on a particular memory process as either positive or negative. Stress is not a unitary process, with its duration, intensity, or timing with regards to the cognitive challenge being critical for its cognitive outcome [1]. In particular, stress intensity has been long recognized in the literature as highly relevant, with the predominant belief that an inverted-U-shaped function can explain the relationship between stress intensity and memory (i.e. low and high stress levels impairing memory, whereas intermediate levels facilitating it). Strikingly, despite the popularity of this hypothesis, experimental evidence supporting the existence of an inverted-U-shaped relationship for performance of rats in a hippocampal learning task under the same experimental conditions was presented only recently [8]. Stress mediators: glucocorticoids and norepinephrineGlucocorticoids and the noradrenergic system have been identified as key mediators of the cognitive effects of stress [1,2,9,10]. Adrenal glucocorticoids, steroid hormones produced by the adrenal glands, can cross the blood-brain barrier, gaining access to the brain. Through the binding to specific receptors, glucocorticoids ca...

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“…Classic genomic actions of glucocorticoids have been implicated in their effects on memory consolidation, a process that normally requires de novo protein synthesis. More recently, rapid nongenomic effects have been implicated in the processing of ongoing information, and thereby as a potential mechanism to affect the processes of acquisition and retrieval of information (13). Strikingly, both genomic and nongenomic actions of glucocorticoids can have an impact on glutamatergic mechanisms in the context of memory processing, including actions through NMDA receptors (13).…”

Section: Underlying Mechanismsmentioning

confidence: 99%

“…More recently, rapid nongenomic effects have been implicated in the processing of ongoing information, and thereby as a potential mechanism to affect the processes of acquisition and retrieval of information (13). Strikingly, both genomic and nongenomic actions of glucocorticoids can have an impact on glutamatergic mechanisms in the context of memory processing, including actions through NMDA receptors (13). There may thus be some convergence between the mechanisms involved in the therapeutical efficacy of D-cycloserine and those of glucocorticoids in their facilitating effects on extinction learning.…”

Section: Underlying Mechanismsmentioning

confidence: 99%