von Dr. Jennifer L. Moore
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| [1.] Jm/Fragment 288 01 - Diskussion Zuletzt bearbeitet: 2014-01-12 21:49:04 Graf Isolan | BauernOpfer, Fragment, Gesichtet, Jm, SMWFragment, Schutzlevel sysop, Wang et al 2008 |
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| Untersuchte Arbeit: Seite: 288, Zeilen: 1-25 |
Quelle: Wang et al 2008 Seite(n): 5607, 5608, Zeilen: 5607: r.col: 18ff; 5608: l.col: 1ff |
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| [However, the effect of postreactivation glucocorticoid on contextual fear memory was reversed by a reminder shock, thereby suggesting that augmentation of single-] trial contextual fear memory extinction is the more likely mechanism for these effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006). Maroun and Akirav (2008), however, provided evidence that stress might have an inhibitory effect on the reconsolidation of recognition memory. They found that in habituated (i.e., high arousal level) and nonhabituated (i.e., low arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of object recognition memory. Further, Zhao and colleagues (2007) were the first to demonstrate that cocaine-conditioned place preference (i.e., context cue memory) was blocked in rats experiencing stress following re-exposure to the previously drug-paired chamber, thereby demonstrating a potential inhibitory effect of stress on the reconsolidation of contextually mediated drug memory.
Extensive evidence suggests that the basolateral amygdala (BLA) is a key region that regulates the effects of stress and glucocorticoids on memory formation, consolidation and reconsolidation (Roozendaal & McGaugh, 1997; Roozendaal et al., 2002; Roozendaal, 2003). Lesions of the BLA block the dexamethasone-induced memory enhancement in an inhibitory avoidance task, suggesting that the BLA is a critical site for the modulatory effect of glucocorticoids on memory formation (Roozendaal & McGaugh, 1996). It has been reported that glucocorticoids in BLA contribute to memory consolidation. Post-training infusions of a GR agonist into the BLA enhance memory performance (Roozendaal & McGaugh, 1997). Immediate postretrieval intra-BLA infusion of RU486 selectively impairs long-term auditory fear memory, suggesting that glucocorticoid receptors in the BLA are required for reconsolidation of auditory fear memory (Jin et al., 2007). Wang and colleagues (2008) also demonstrated that a GR antagonist infused into the BLA reversed the inhibitory effect of post-reactivation stress on a morphine reward memory. This finding suggests that activation of GRs in the BLA plays a critical role in the effects of postreactivation stress on context-cue dependent drug-related memory. |
However, the effect of postreactivation glucocorticoid on contextual fear memory is reversed by a reminder shock. This finding suggests that augmentation of single-trial contextual fear memory extinc-
[page 5608] tion is the more likely mechanism for the effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006). Maroun and Akirav (2008) provided the first evidence that stress might have an inhibitory effect on the reconsolidation of memory. They found that in habituated (high arousal level) and nonhabituated (low arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of objective recognition memory (Maroun and Akirav, 2007). Our previous study was the first to demonstrate that cocaine CPP was blocked in rats experiencing stress after re-exposure to the previously drug-paired chamber, showing a potential inhibitory effect of stress on reconsolidation of drug-related memory (Zhao et al., 2007). [...] [...] Likewise, extensive evidence suggests that the BLA is a key region that regulates the effects of stress and glucocorticoids on memory formation, consolidation, and reconsolidation (Roozendaal and McGaugh, 1997; Roozendaal et al., 2002; Roozendaal, 2003). Lesions of the BLA, but not the CeA, block the dexamethasone-induced memory enhancement in an inhibitory avoidance task, suggesting that the BLA is a critical site for the modulatory effect of glucocorticoids on memory formation (Roozendaal and McGaugh, 1996). It has been reported that glucocorticoids in BLA, but not the CeA, contribute to memory consolidation. Post-training infusions of a GR agonist into the BLA, but not into the CeA, enhance memory performance (Roozendaal and McGaugh, 1997). Immediate postretrieval intra-BLA infusion of RU486 selectively impairs long-term auditory fear memory, suggesting that glucocorticoid receptors in the BLA are required for reconsolidation of auditory fear memory (Jin et al., 2007). Consistent with previous studies, we showed that aGR agonist injected into the BLA, but not into the CeA, after memory reactivation mimics the effects of postreactivation stress. Moreover, we demonstrated that a GR antagonist infused into the BLA, but not into the CeA, reversed the inhibitory effect of postreactivation stress on a morphine reward memory. This finding suggests that activation of GRs in the BLA plays a critical role in the effects of postreactivation stress on drug-related memory. |
It is clear to the reader that here the research of others is presented including the research of Wang et al. (2008). It is not clear however, that this presentation is taken from Wang et al. (2008) in its entirety, only making minor adjustments. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Graf Isolan, Zeitstempel: 20140112215052