Post-training administration of corticosterone enhances consolidation of contextual fear memory and hippocampal long-term potentiation in rats

Abrari, Kataneh; Rashidy-Pour, Ali; Semnanian, Saeed; Fathollahi, Yaghoub

doi:10.1016/j.nlm.2008.10.008

Cited by 62 publications

(38 citation statements)

References 49 publications

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“…Furthermore, Cordero and Sandi, (1998) demonstrated that rats which were fear conditioned with a low intensity shock and then injected with corticosterone immediately afterwards, showed more freezing than controls 24 h and 7 days following conditioning. These glucocorticoid effects tend to be biphasic whereby low to moderate doses enhance, while high doses inhibit consolidation of fear memory (Pugh et al, 1997;Abrari et al, 2009). Overall, these data suggest that glucocorticoids play an important role in the consolidation of a shock-induced fear memory.…”

Section: Fear Conditioning Consolidation and Glucocorticoidsmentioning

confidence: 78%

Glucocorticoids are required for extinction of predator stress-induced hyperarousal

Clay

Hebert

Gill

et al. 2011

Neurobiology of Learning and Memory

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Extinction of fearful behavior induced by severe stress was studied using predator stress. Predator stress involves a ten minute unprotected exposure of a rodent to a cat which induces long-lasting changes in anxiety-like behaviours and hyperarousal (increased acoustic startle response) (Adamec & Shallow, 1993; Adamec et al., 200 I;Cohen et al., 2004). In the present set of experiments, three questions were addressed using predator stressed mice. First, can predator stress-induced fear memories be extinguished? Second, is the extinction of predator stress-induced fear memories glucocorticoid-dependent? Finally, is re-exposure to the predator stress context necessary to see glucocorticoid's effects on predator stress-induced fear memories?Extinction was induced by re-exposing mice to the predator stress room in the absence of the cat. This repeated re-exposure to predator stress context increased activity in the predator stress context implying extinction of predator stress-induced immobility, a context-dependent fear memory. Repeated re-exposures to the predator stress context also decreased subsequent hyperarousal (acoustic startle response) and generalized anxiety-like behaviour. These fearful behaviors were predator stress context independent, having been tested in environments different from the cat exposure room. Furthermore, blocking glucocorticoid synthesis with metyrapone during repeated exposures to the predator stress context had no effect on activity. Therefore, reducing corticosterone levels did not affect extinction of the predator stress-induced, context-dependent fear memory.However, metyrapone given during repeated exposures to the predator stress context prevented extinction of predator stress-induced hyperarousal. These results suggest that extinction of predator stress-induced, context-independent fear memory is dependent on Ill the presence of endogenous corticosterone during the extinction trial . Finally, reexposure to the predator stress context was found to be necessary to see glucocorticoid's effects on predator stress-induced fear memories. This was determined by repeated injection of metyrapone over days without re-exposure to the predator stre s context.

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Section: Fear Conditioning Consolidation and Glucocorticoidsmentioning

confidence: 78%

Glucocorticoids are required for extinction of predator stress-induced hyperarousal

Clay

Hebert

Gill

et al. 2011

Neurobiology of Learning and Memory

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“…Furthermore, animals administered the construct before fear conditioning demonstrate suppressed recall for conditioning [53], consistent with the sex differences in the study described earlier. As GCs have been shown to enhance memory for conditioned fear [54], these studies together suggest that estrogen is in a position to negate some of the potentially harmful effects of stress in the amygdala by suppressing the strengthened memory. Prolonged or enhanced memory for an aversive event can lead to inappropriate responses to relevant cues in the future, when no real danger exists.…”

Section: Estrogen-stress Interactions In the Amygdalamentioning

confidence: 85%

Estrogen, stress and the brain: progress toward unraveling gender discrepancies in major depressive disorder

Shansky

2009

Expert Review of Neurotherapeutics

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Women are twice as likely as men to develop major depressive disorder (MDD) and, while the neurobiological factors underlying this discrepancy are yet to be identified, estrogen almost certainly plays a role. MDD can be precipitated or exacerbated by exposure to stress and there is substantial evidence to suggest that estrogen can interact with stress systems to produce unique stress effects in females. This review integrates current research in animal models regarding estrogen-stress interactions in three areas of the brain known to be relevant to MDD: the hippocampus, the amygdala and the prefrontal cortex. The results from these studies are discussed in the context of MDD, and their implications for future treatment of MDD in women are explored.

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“…There is evidence that LTP is enhanced via MR activation and reduced or even turned into LTD after GR activation (Pavlides et al, 1993(Pavlides et al, , 1994(Pavlides et al, , 1995Smriga et al, 1996;Yamada et al, 2003;Avital et al, 2006;Vouimba et al, 2007;Yarom et al, 2008), similar to what has been described for the CA1 area. Abrari et al (2009) reported facilitated induction of LTP in association with improved memory when rats were treated with a moderately high dose of corticosterone directly after training in a fear conditioning paradigm. However, others found no change after inescapable or cold stress (Shors and Dryver, 1994;Vouimba et al, 2004) or could not link stress-induced changes in LTP/LTD to known corticosteroid receptor types (Spyrka et al, 2011).…”

Section: B Slow Modulation Of Synaptic Plasticitymentioning

confidence: 99%

Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

2012

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Post-training administration of corticosterone enhances consolidation of contextual fear memory and hippocampal long-term potentiation in rats

Cited by 62 publications

References 49 publications

Glucocorticoids are required for extinction of predator stress-induced hyperarousal

Glucocorticoids are required for extinction of predator stress-induced hyperarousal

Estrogen, stress and the brain: progress toward unraveling gender discrepancies in major depressive disorder

Unraveling the Time Domains of Corticosteroid Hormone Influences on Brain Activity: Rapid, Slow, and Chronic Modes

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