Memory enhancement of classical fear conditioning by post-training injections of corticosterone in rats

Hui, Gabriel K.; Figueroa, Isabel; Poytress, Bonnie S.; Roozendaal, Benno; McGaugh, James L.; Weinberger, Norman M.

doi:10.1016/j.nlm.2003.09.002

Cited by 152 publications

(95 citation statements)

References 53 publications

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“…Thus, the level of stress applied in our experiment is apparently in the range that provokes a facilitation of memory retention. This was found to be the case in a variety of emotionally arousing tasks, such as inhibitory avoidance, spatial learning, discrimination learning, and fear conditioning (Cordero and Sandi, 1998;Flood et al, 1978;Hui et al, 2004;Kovacs et al, 1977;Pugh et al, 1997;Roozendaal and McGaugh, 1996;Sandi et al, 1997).…”

Section: Opposite Effect Of the Stressor On The Consolidation Of Recomentioning

confidence: 87%

Arousal and Stress Effects on Consolidation and Reconsolidation of Recognition Memory

Maroun

Akirav

2007

Neuropsychopharmacol

118

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This study examined the effects of the arousal level of the rat and exposure to a behavioral stressor on consolidation and reconsolidation of a nonaversive learning paradigm, the object recognition task. Learning was tested under two arousal conditions: no previous habituation to the experimental context (high novelty stress/arousal level) or extensive prior habituation (reduced novelty stress/arousal level). Results indicated that in the habituated rats, exposure to an out-of-context stressor (ie, elevated platform stress) impaired longterm consolidation and reconsolidation of object recognition. RU-486, a glucocorticoid receptor (GR) antagonist, infused into the basolateral amygdala (BLA), reversed the impairing effects of the stressor. In contrast, the nonhabituated aroused rats were impaired when consolidation was examined, but their memory was intact following reactivation of the memory trace. Exposure of nonhabituated rats to an out-of-context stressor enhanced the long-term consolidation of recognition memory, but impaired reconsolidation, and the effects were reversed by a GR antagonist infused into the BLA. Additionally, nonhabituated control rats showed intact retrieval following microinfusion of propranolol to the BLA immediately after the training, suggesting an involvement of beta-adrenoceptors in the BLA in the arousal-induced impairment of consolidation. These findings demonstrate opposite effects, detrimental and facilitative, of arousal and stress on memory consolidation and reconsolidation. In addition, the data suggests that although some general features underlie consolidation and reconsolidation, there is a possible dissimilarity between the two processes, which is dependent on the arousal level of the animal during training.

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Section: Opposite Effect Of the Stressor On The Consolidation Of Recomentioning

confidence: 87%

Arousal and Stress Effects on Consolidation and Reconsolidation of Recognition Memory

Maroun

Akirav

2007

Neuropsychopharmacol

118

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“…This is in sharp contrast to adult CORT effects in which CORT enhances/attenuates fear-conditioning and inhibitory conditioning, but CORT blockade does not lead to a hedonic reversal and resulting preference (Corodimas et al, 1994;Roozendaal et al, 1996Roozendaal et al, , 2002Pugh et al, 1997;Hui et al, 2004;Thompson et al, 2004). We have hypothesized previously that the unique characteristics of the neonatal noradrenergic system may create a default odor preference tendency in neonates.…”

Section: Contrasting Role Of Cort In Infants and Adultsmentioning

confidence: 88%

Dual Circuitry for Odor-Shock Conditioning during Infancy: Corticosterone Switches between Fear and Attraction via Amygdala

Moriceau

Wilson

Levine

et al. 2006

Journal of Neuroscience

205

231

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Rat pups must learn maternal odor to support attachment behaviors, including nursing and orientation toward the mother. Neonates have a sensitive period for rapid, robust odor learning characterized by increased ability to learn odor preferences and decreased ability to learn odor aversions. Specifically, odor-0.5 mA shock association paradoxically causes an odor preference and coincident failure of amygdala activation in pups until postnatal day 10 (P10). Because sensitive-period termination coincides with a declining "stress hyporesponsive period" when corticosterone release is attenuated, we explored the role of corticosterone in sensitive-period termination. Odor was paired with 0.5 mA shock in either sensitive-period (P8) or postsensitive-period (P12) pups while manipulating corticosterone. We then assessed preference/aversion learning and the olfactory neural circuitry underlying its acquisition. Although sensitive-period control paired odor-shock pups learned an odor preference without amygdala participation, systemic (3 mg/kg, i.p.; 24 h and 30 min before training) or intra-amygdala corticosterone (50 or 100 ng; during training) permitted precocious odor-aversion learning and evoked amygdala neural activity similar to that expressed by older pups. In postsensitive-period (P12) pups, control paired odor-shock pups showed an odor aversion and amygdala activation, whereas corticosterone-depleted (adrenalectomized) paired odor-shock pups showed odor-preference learning and activation of an odor learning circuit characteristic of the sensitive period. Intra-amygdala corticosterone receptor antagonist (0.3 ng; during training) infused into postsensitive-period (P12) paired odor-shock pups also showed odor-preference learning. These results suggest corticosterone is important in sensitive-period termination and developmental emergence of olfactory fear conditioning, acting via the amygdala as a switch between fear and attraction. Because maternal stimulation of pups modulates the pups' endogenous corticosterone, this suggests maternal care quality may alter sensitive-period duration.

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“…Corticosterone also exerts effects within the amygdala via actions at glucocorticoid receptors (Aronsson et al, 1988). Of particular interest in this context, BLA has been identified as a critical site of action through which glucocorticoids modulate associative fear memory, (for example) glucocorticoid receptor agonists administered systemically or directly into the BLA enhance fear conditioning in rats (Zorawski and Killcross, 2002;Hui et al, 2004;Roozendaal et al, 2006). This raises the possibility that increased glucocorticoid receptor activity in smaller BLA mice may be a factor driving enhanced fear conditioning, although this remains to be tested.…”

Section: Discussionmentioning

confidence: 99%

Variation in Mouse Basolateral Amygdala Volume is Associated With Differences in Stress Reactivity and Fear Learning

Yang

Mozhui

Karlsson

et al. 2008

Neuropsychopharmacol

129

106

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A wealth of research identifies the amygdala as a key brain region mediating negative affect, and implicates amygdala dysfunction in the pathophysiology of anxiety disorders. Although there is a strong genetic component to anxiety disorders such as posttraumatic stress disorder (PTSD) there remains debate about whether abnormalities in amygdala function predispose to these disorders. In the present study, groups of C57BL/6 Â DBA/2 (B Â D) recombinant inbred strains of mice were selected for differences in volume of the basolateral amygdala complex (BLA). Strains with relatively small, medium, or large BLA volumes were compared for Pavlovian fear learning and memory, anxiety-related behaviors, depression-related behavior, and glucocorticoid responses to stress. Strains with relatively small BLA exhibited stronger conditioned fear responses to both auditory tone and contextual stimuli, as compared to groups with larger BLA. The small BLA group also showed significantly greater corticosterone responses to stress than the larger BLA groups. BLA volume did not predict clear differences in measures of anxiety-like behavior or depression-related behavior, other than greater locomotor inhibition to novelty in strains with smaller BLA. Neither striatal, hippocampal nor cerebellar volumes correlated significantly with any behavioral measure. The present data demonstrate a phenotype of enhanced fear conditioning and exaggerated glucocorticoid responses to stress associated with small BLA volume. This profile is reminiscent of the increased fear processing and stress reactivity that is associated with amygdala excitability and reduced amygdala volume in humans carrying loss of function polymorphisms in the serotonin transporter and monoamine oxidase A genes. Our study provides a unique example of how natural variation in amygdala volume associates with specific fear-and stress-related phenotypes in rodents, and further supports the role of amygdala dysfunction in anxiety disorders such as PTSD.

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Memory enhancement of classical fear conditioning by post-training injections of corticosterone in rats

Cited by 152 publications

References 53 publications

Arousal and Stress Effects on Consolidation and Reconsolidation of Recognition Memory

Arousal and Stress Effects on Consolidation and Reconsolidation of Recognition Memory

Dual Circuitry for Odor-Shock Conditioning during Infancy: Corticosterone Switches between Fear and Attraction via Amygdala

Variation in Mouse Basolateral Amygdala Volume is Associated With Differences in Stress Reactivity and Fear Learning

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