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Angaben zur Quelle [Bearbeiten]

Autor     Xiao-Yi Wang, Mei Zhao, Udi E. Ghitza, Yan-Qin Li, Lin Lu
Titel    Stress Impairs Reconsolidation of Drug Memory via Glucocorticoid Receptors in the Basolateral Amygdala
Zeitschrift    The Journal of Neuroscience
Datum    21. May 2008
Jahrgang    28
Nummer    21
Seiten    5602–5610
URL    http://www.jneurosci.org/content/28/21/5602.full.pdf

Literaturverz.   

yes
Fußnoten    yes
Fragmente    5


Fragmente der Quelle:
[1.] Jm/Dublette/Fragment 005 04 - Diskussion
Zuletzt bearbeitet: 2014-01-13 08:37:44 Klgn
Dublette, Fragment, Gesichtet, Jm, KeineWertung, SMWFragment, Schutzlevel sysop, Wang et al 2008

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Stress and glucocorticoids (GCs) both enhance (Loscertales et al., 1998; Roozendaal, 2002) as well as impair (Diamond et al., 1996; Newcomer et al., 1994, 1999) memory consolidation, and memory retrieval is typically impaired (de Quervain et al., 1998; Kuhlmann et al., 2005). To date, only a few groups have studied the effects of stress or GCs on the reconsolidation of memory. Maroun and Akirav (2008) provided the first evidence that stress may exert an inhibitory effect on the reconsolidation of memory. They found that, in habituated (low arousal level) and nonhabituated (high arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of object recognition memory. Stress and glucocorticoids enhance (Loscertales et al., 1998; Roozendaal, 2002) as well as impair (Newcomer et al., 1994; Diamond et al., 1996; Newcomer et al., 1999) memory consolidation. In contrast, memory retrieval is usually impaired with high circulating levels of glucocorticoids or after injections of glucocorticoid receptor (GR) agonists into different brain regions (de Quervain et al., 1998, 2000; Kuhlmann et al., 2005).

[page 5607]

Only a few groups have studied the effects of stress or glucocorticoids on reconsolidation of memory.

[5608]

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).

Anmerkungen

Wang et al. is mentioned just after the documented fragment, but in relation to their own results, not as a reference for the copied text.

Probably the better match can be found here: Jm/Fragment_005_01

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[2.] Jm/Fragment 004 05 - Diskussion
Zuletzt bearbeitet: 2014-02-20 00:17:35 Schumann
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Using drug cues as reinforcers, investigators reported that the β-adrenoreceptor antagonist propranolol, administered after reactivation of cocaine or morphine conditioned place preference (CPP), impairs drug seeking via disruption of reconsolidation (Bernardi et al., 2006; Robinson & Franklin, 2007). Using drugs as reinforcers, investigators reported that the β-adrenoreceptor antagonist propranolol, administered after reactivation of cocaine or morphine conditioned place preference (CPP), impairs drug seeking via disruption of reconsolidation (Bernardi et al., 2006; Robinson and Franklin, 2007).
Anmerkungen

The source is not mentioned here.

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[3.] Jm/Fragment 004 19 - Diskussion
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Morphine CPP is persistently disrupted when anisomycin, a protein synthesis inhibitor, is administered after a conditioning session (Milekic et al., 2006). When mice previously conditioned for cocaine place preference are re-exposed to cocaine in the drug-paired compartment after systemic administration of SL327, an inhibitor of ERK (extracellular signal-regulated protein kinase) activation, CPP response is abolished (Valjent et al., 2006). Together, drug-related memory can be inhibited or erased by interrupting its reconsolidation process. Morphine CPP is persistently disrupted when anisomycin, a protein synthesis inhibitor, is administered after a conditioning session (Milekic et al., 2006). When mice previously conditioned for cocaine place preference are re-exposed to cocaine in the drug-paired compartment after systemic administration of SL327 [α-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl) benzeneacetonitrile], an inhibitor of ERK (extracellular signal-regulated protein kinase) activation, CPP response is abolished (Valjent et al., 2006a). Together, drug-related memory can be inhibited or erased by interrupting its reconsolidation process.
Anmerkungen

The source is not mentioned here, only on the next page in a different context.

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[4.] Jm/Fragment 287 22 - Diskussion
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Cai and colleagues (2006) reported that when glucocorticoids were administered immediately after reactivation of a contextual fear memory, subsequent recall was significantly diminished. However, the effect of postreactivation glucocorticoid on contextual fear memory was reversed by a reminder shock, thereby suggesting that augmentation of single- [page 288] trial contextual fear memory extinction is the more likely mechanism for these effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006). Cai et al. (2006) reported that when glucocorticoids are administered immediately after reactivation of a contextual fear memory, subsequent recall is significantly diminished. 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).

Anmerkungen

The source is not mentioned in the context of this text fragment.

Continued on the next page: Jm/Fragment_288_01

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[5.] Jm/Fragment 288 01 - Diskussion
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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.

Anmerkungen

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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(Hindemith) Agrippina1

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