Acute stress-induced impairment of spatial memory is associated with decreased expression of neural cell adhesion molecule in the hippocampus and prefrontal cortex

Sandi, Carmen; Woodson, James C.; Haynes, Vernon F.; Park, Collin R.; Touyarot, Katia; López-Fernández, Miguel A.; Venero, César; Diamond, David M.

doi:10.1016/j.biopsych.2004.12.034

Cited by 109 publications

(90 citation statements)

References 98 publications

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“…Acute exposure to predator odor impairs working memory, a result consistent with alterations in mesoprefontal dopamine activity (Morrow et al 2000). Additional work has shown that acute predator stress impairs long-term hippocampal-dependent spatial memory and this impairment is associated with altered gene expression in the hippocampus and the prefrontal cortex (Diamond et al 1999;Sandi et al 2005;Woodson et al 2003). The ability of predator stress to facilitate recall of and responsiveness to a previously conditioned context is another novel finding of this study.…”

Section: Conditioned Locomotor Arousalsupporting

confidence: 63%

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Schiltz

Kelley

Landry

2007

Biological Psychiatry

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Section: Conditioned Locomotor Arousalsupporting

confidence: 63%

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Schiltz

Kelley

Landry

2007

Biological Psychiatry

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“…The resulting downstream processes might be reversed by antidepressants including lithium (55,79), tianeptine, and agomelatine (28,63), potentially via cellular cascades including neural cell adhesion molecules (47,79).…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms by which CRH results in rapid loss of spines are not fully understood. Although the final step includes disintegration of spine cytoskeleton (54), upstream mechanisms might involve cellular adhesion molecules (79) and/or tissue-plasminogen activator (40). In addition, the basis for the region specificity of the CRH-dependent stress-induced changes found here remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling

Chen¹,

Rex

Rice

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

239

206

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Stress affects the hippocampus, a brain region crucial for memory. In rodents, acute stress may reduce density of dendritic spines, the location of postsynaptic elements of excitatory synapses, and impair long-term potentiation and memory. Steroid stress hormones and neurotransmitters have been implicated in the underlying mechanisms, but the role of corticotropin-releasing hormone (CRH), a hypothalamic hormone also released during stress within hippocampus, has not been elucidated. In addition, the causal relationship of spine loss and memory defects after acute stress is unclear. We used transgenic mice that expressed YFP in hippocampal neurons and found that a 5-h stress resulted in profound loss of learning and memory. This deficit was associated with selective disruption of long-term potentiation and of dendritic spine integrity in commissural/associational pathways of hippocampal area CA3. The degree of memory deficit in individual mice correlated significantly with the reduced density of area CA3 apical dendritic spines in the same mice. Moreover, administration of the CRH receptor type 1 (CRFR 1 ) blocker NBI 30775 directly into the brain prevented the stress-induced spine loss and restored the stress-impaired cognitive functions. We conclude that acute, hours-long stress impairs learning and memory via mechanisms that disrupt the integrity of hippocampal dendritic spines. In addition, establishing the contribution of hippocampal CRH-CRFR 1 signaling to these processes highlights the complexity of the orchestrated mechanisms by which stress impacts hippocampal structure and function.corticotropin-releasing factor| long-term potentiation | memory | synaptic plasticity | hippocampus T he hippocampal formation is involved in a circuit that is required for several types of memory in both humans and rodents (1-4). At the physiological/cellular level, memory processes generally are believed to involve long-term potentiation (LTP) of synaptic function (5-8). This potentiation, in turn, is associated with an increase in the size (9, 10) and altered composition (11-13) of dendritic spines of hippocampal principal cells that carry excitatory synapses (14, 15).Stress affects both the function and the structure of the hippocampus (16)(17)(18)(19)(20)(21)(22)(23)(24)(25). A large body of work has demonstrated that chronic stress may result in memory deficits (26-31) and abnormal LTP (32-34), and these functional deficits often are accompanied by diminished dendritic arborization (35-42). Short-term or acute stress, lasting minutes to hours, also has been found to affect memory (43-47). In parallel, short-term stress has been reported to influence LTP (48-52) and reduce the density of dendritic spines in area CA1 (44, 53) or area CA3 (51, 54). Whereas hippocampus-mediated memory deficits commonly were associated with-and perhaps result from-loss of synapse-bearing dendrites and dendritic spines, this association has not been universal (37,46,55), so that the structure-function relationship underlying the effects of st...

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“…Such disruptive effects have been shown to occur when stress is applied 30 min before a retention session, 24 h after training animals in the water maze (de Quervain, Roozendaal, & McGaugh, 1998) and when it is applied during the 30 min before testing in a radial arm water maze under a protocol in which learning was applied on the same day just before both, stress and retention testing (Diamond, Park, Heman, & Rose, 1999;Sandi et al, 2005;Woodson, Macintosh, Fleshner, & Diamond, 2003). Glucocorticoids were implicated in the impairing effect of stress, with increasing corticosterone levels being necessary and sufficient (though interacting with noradrenergic mechanisms in the basolateral amygdala) to impair retrieval when animals were tested 24 h after training (de Quervain et al, 1998;Roozendaal, Griffith, Buranday, De Quervain, & McGaugh, 2003;Roozendaal, Hahn, Nathan, de Quervain, & McGaugh, 2004).…”

Section: Extrinsic Stress and Ncammentioning

confidence: 99%

Learning under stress: A role for the neural cell adhesion molecule NCAM

Bisaz

Conboy

Sandi

2009

Neurobiology of Learning and Memory

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a b s t r a c tStress is known to be a potent modulator of brain function and cognition. While prolonged and/or excessive stress generally exerts negative effects on learning and memory processes, acute stress can have differential effects on memory function depending on a number of factors (such as stress duration, stress intensity, timing and the source of the stress, as well as the learning type under study). Here, we have focused on the effects of 'acute' stress, and examined the literature attending to whether the ''source of stress" is 'intrinsic' (i.e., when stress is originated by the cognitive task) or 'extrinsic' (i.e., when stress is induced by elements not related to the cognitive task). We have questioned here whether the neural cell adhesion molecule of the immunoglobulin superfamily (NCAM) contributes to the neurobiological mechanisms that translate the effects of these two different stress sources into the different behavioral and cognitive outcomes. NCAM is a cell adhesion macromolecule known to play a critical role in development and plasticity of the nervous system. NCAM and its post-translational modified form PSA-NCAM are critically involved in mechanisms of learning and memory and their expression levels are known to be highly susceptible to modulation by stress. Whereas available data are insufficient to conclude as to whether NCAM mediates extrinsic stress effects on learning and memory processes, we present systematic evidence supporting a key mediating role for both NCAM and PSA-NCAM in the facilitation of memory consolidation induced by intrinsic stress. Furthermore, NCAM is suggested to participate in some of the bidirectional effects of stress on memory processes, with its enhanced synaptic expression involved in facilitating stress actions while its reduced expression being related to impairing effects of stress on memory function.

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Acute stress-induced impairment of spatial memory is associated with decreased expression of neural cell adhesion molecule in the hippocampus and prefrontal cortex

Cited by 109 publications

References 98 publications

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Acute Stress and Nicotine Cues Interact to Unveil Locomotor Arousal and Activity-Dependent Gene Expression in the Prefrontal Cortex

Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling

Learning under stress: A role for the neural cell adhesion molecule NCAM

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