Chronic psychosocial stress impairs learning and memory and increases sensitivity to yohimbine in adult rats

Park, Collin R.; Campbell, Adam M.; Diamond, David M.

doi:10.1016/s0006-3223(01)01255-0

Cited by 146 publications

(97 citation statements)

References 97 publications

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“…Therefore, chronic high levels of the hormone corticosterone, which is released by the adrenal glands after HPA axis activation, could produce permanent changes in response to stressors long after the CORT exposure has ended. Indeed, several studies have shown that chronic stress or the presence of an anxiety disorder can increase sensitivity to the effects of yohimbine (Charney et al, 1984;Park et al, 2001;Rosen et al, 1999;Zoladz et al, 2008). However, the majority of differences in impulsivity observed here are unlikely to be explained by altered HPA axis function, but rather by long-lasting neuroplasticity in the circuits that regulate impulsive behavior and decision-making.…”

Section: Discussionmentioning

confidence: 62%

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Torregrossa

Xie

Taylor

2012

Neuropsychopharmacol

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Chronic stress during adolescence is associated with an increased risk for alcoholism and addictive disorders. Addiction is also associated with increased impulsivity, and stress during adolescence could alter cortical circuits responsible for response inhibition. Therefore, the present study determined the effect of chronic exposure to the stress hormone corticosterone (CORT) during adolescence on tests of impulsivity in adulthood and examined possible biochemical mechanisms. Male Sprague-Dawley rats were exposed to CORT by their drinking water during adolescence (post-natal day 30-50). The rats were then tested in adulthood to assess behavior on the 5-choice serial reaction time task (5CSRTT), stop-signal reaction time task (SSRTT), and the delay-discounting task, which differentially assess attention, impulsive action, and impulsive choice. Yohimbine-induced impulsivity on the 5CSRTT and biochemical analysis of the lateral orbital frontal cortex (lOFC) was also assessed owing to the ability of yohimbine to activate the hypothalamic-pituitary-adrenal axis and influence impulsivity. Adolescent CORT-treated rats were found to behave largely like controls on the 5CSRTT, but did show reduced premature responses when the intertrial interval was increased. Nevertheless, the CORT-treated rats tended to have more yohimbineinduced impulsive responses at low doses on this task, which was not found to be due to increased pCREB in the lOFC, but could be related to a higher expression/activity of the AMPA receptor subunit GluR1. Adolescent CORT-treated rats performed more accurately on the SSRTT, but showed greater impulsivity on the delay-discounting task, as indicated by steeper discounting functions. Therefore, adolescent CORT exposure reduced impulsive action but increased impulsive choice, indicating that chronic stress hormone exposure in adolescence can have long-term consequences on behavior.

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Section: Discussionmentioning

confidence: 62%

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Torregrossa

Xie

Taylor

2012

Neuropsychopharmacol

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“…Stress may have enhanced performance by interfering with habituation to the novel arm. This interpretation is supported by impaired habituation to novel environments in male rats following psychosocial stress (Park et al, 2001). Another interpretation is that chronic stress facilitated females' spatial memory, similar to the facilitative effects found in the radial arm maze and object placement tasks (Bowman et al, 2001(Bowman et al, , 2002Beck and Luine, 2002).…”

Section: Effects Of Chronic Stress On the Y-mazementioning

confidence: 93%

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

et al. 2005

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Emerging data report sex differences in how the brain responds to chronic stress. Here, we investigated the effects of chronic restraint stress (6 h/day/21 days) on hippocampal morphology and function in ovariectomized female rats. Chronic restraint stress caused CA3 apical dendritic retraction in short-and long-shafted neurons, while it reduced basal dendritic arbors in long-shafted neurons only. Chronic restraint did not affect CA1 dendritic arborization, although it increased the proportion of CA1 spine heads compared with controls. Both stressed and control animals performed well on the Y-maze, a spatial memory task. However, chronic stress enhanced Y-maze performance compared with controls, which may reflect facilitated spatial memory or reduced habituation. Ymaze performance correlated with CA1 spine head proportion. This relationship suggests that spatial ability in females may be more tightly coupled with CA1 morphology, which may override the influence of CA3 dendritic retraction. Thus, this research provides additional evidence that CA3 morphology does not always parallel spatial memory.

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“…A large body of work has demonstrated that chronic stress may result in memory deficits (26)(27)(28)(29)(30)(31) and abnormal LTP (32)(33)(34), and these functional deficits often are accompanied by diminished dendritic arborization (35)(36)(37)(38)(39)(40)(41)(42). Short-term or acute stress, lasting minutes to hours, also has been found to affect memory (43)(44)(45)(46)(47).…”

mentioning

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.

232

199

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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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Chronic psychosocial stress impairs learning and memory and increases sensitivity to yohimbine in adult rats

Cited by 146 publications

References 97 publications

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

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

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