No erasure effect of retrieval–extinction trial on fear memory in the hippocampus-independent and dependent paradigms

Ishii, Daisuke; Matsuzawa, Daisuke; Matsuda, Shingo; Tomizawa, Haruna; Sutoh, Chihiro; Shimizu, Eiji

doi:10.1016/j.neulet.2012.06.048

Cited by 37 publications

(35 citation statements)

References 13 publications

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“…These findings are consistent with those indicating that extinction shortly after fear learning or fear cue exposure impairs extinction and exacerbates spontaneous recovery, renewal, and reinstatement (Morris et al 2005;Chan et al 2010;Costanzi et al 2011;Ishii et al 2012). Other studies have found opposing results-that extinction soon after acquisition (Myers et al 2006) or retrieval (Monfils et al 2009) promotes the retention of extinction (see Flavell et al 2011).…”

Section: Discussionsupporting

confidence: 90%

“…Further, some studies have shown similar effects to those of Monfils et al (2009) using contextual fear preparations in mice (Rao-Ruiz et al 2011) while others show findings like ours in contextual paradigms (Ishii et al 2012). Although important to study, it is unlikely that the discrepant findings in the literature are simply due to procedural differences, such as the type of fear conditioning (cued or contextual), the postsession delay (immediate or 10 min), or differences in species.…”

Section: Discussionsupporting

confidence: 69%

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Exposure to a fearful context during periods of memory plasticity impairs extinction via hyperactivation of frontal-amygdalar circuits

et al. 2013

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An issue of increasing theoretical and translational importance is to understand the conditions under which learned fear can be suppressed, or even eliminated. Basic research has pointed to extinction, in which an organism is exposed to a fearful stimulus (such as a context) in the absence of an expected aversive outcome (such as a shock). This extinction process results in the suppression of fear responses, but is generally thought to leave the original fearful memory intact. Here, we investigate the effects of extinction during periods of memory lability on behavioral responses and on expression of the immediate -early gene c-Fos within fear conditioning and extinction circuits. Our results show that long-term extinction is impaired when it occurs during time periods during which the memory should be most vulnerable to disruption (soon after conditioning or retrieval). These behavioral effects are correlated with hyperactivation of medial prefrontal cortex and amygdala subregions associated with fear expression rather than fear extinction. These findings demonstrate that behavioral experiences during periods of heightened fear prevent extinction and prolong the conditioned fear response.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 69%

Exposure to a fearful context during periods of memory plasticity impairs extinction via hyperactivation of frontal-amygdalar circuits

et al. 2013

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“…It has been reported that even administering a single retrieval trial shortly before fear extinction training can lead to persistent attenuation of fear memories in both rodents and human subjects (Monfils et al 2009;Clem and Huganir 2010;Schiller et al 2010). Exposure to a single retrieval trial with the subsequent ability to suppress renewal or spontaneous recovery of fear would have significant clinical implications for behavioral therapy regimes; however, these findings have not been universally accepted, with several recent studies failing to replicate the original findings (Chan et al 2010;Costanzi et al 2011;Ishii et al 2012). In our control experiments we also examined whether an isolated retrieval trial before the extinction session could suppress spontaneous recovery (in the extinction context [ Fig.…”

Section: Discussionmentioning

confidence: 99%

Potentiating mGluR5 function with a positive allosteric modulator enhances adaptive learning

Zhu

Kraniotis

et al. 2013

Learn. Mem.

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Metabotropic glutamate receptor 5 (mGluR5) plays important roles in modulating neural activity and plasticity and has been associated with several neuropathological disorders. Previous work has shown that genetic ablation or pharmacological inhibition of mGluR5 disrupts fear extinction and spatial reversal learning, suggesting that mGluR5 signaling is required for different forms of adaptive learning. Here, we tested whether ADX47273, a selective positive allosteric modulator (PAM) of mGluR5, can enhance adaptive learning in mice. We found that systemic administration of the ADX47273 enhanced reversal learning in the Morris Water Maze, an adaptive task. In addition, we found that ADX47273 had no effect on single-session and multi-session extinction, but administration of ADX47273 after a single retrieval trial enhanced subsequent fear extinction learning. Together these results demonstrate a role for mGluR5 signaling in adaptive learning, and suggest that mGluR5 PAMs represent a viable strategy for treatment of maladaptive learning and for improving behavioral flexibility.

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“…Preliminary unpublished findings from our laboratory indicate that a single post-retrieval extinction session was not sufficient to reduce renewal of cocaine seeking in a self-administration paradigm (number of lever presses during renewal test: No Ret ¼ 53 ± 12, Ret ¼ 49±10; n ¼ 2 and 3 for No Ret and Ret groups, respectively), whereas Xue et al (2012) showed that repeated post-retrieval extinction sessions attenuated renewal of cocaine and heroin self-administration. Lastly, some studies have shown that post-retrieval extinction was not effective at reducing fear or reward-related memories (Perez-Cuesta and Maldonado, 2009;Chan et al, 2010;Costanzi et al, 2011;Flavell et al, 2011;Ishii et al, 2012;Ma et al, 2012;Millan et al, 2013), although specific methodological and boundary conditions (species differences; behavioral paradigm used; type of reinforcer; length of conditioning, retrieval and/or extinction; time between retrieval and extinction training) may explain the divergent results between studies. Ma et al (2012) recently reported that post-retrieval extinction does not completely erase morphine-related memories, as morphine CPP was reinstated by a priming injection following 4 weeks (but not at 1 week) of abstinence.…”

Section: Limitations Of Post-retrieval Extinctionmentioning

confidence: 99%

“…Subsequent studies in other laboratories have shown that post-retrieval extinction reduces fear and reward-related memories in both animals and humans (Clem and Huganir, 2010;Schiller et al, 2010;Flavell et al, 2011;Rao-Ruiz et al, 2011;Xue et al, 2012), indicating that these methods have the potential to be translated into clinical applications. However, other studies have failed to replicate such findings in fear-related memories (Chan et al, 2010;Costanzi et al, 2011;Ishii et al, 2012). Additionally, reports have challenged the reconsolidation theory behind post-retrieval extinction (Millan et al, 2013) and the notion that memories are completely erased following postretrieval extinction (Ma et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Post-Retrieval Extinction Attenuates Cocaine Memories

Sartor

Aston‐Jones

2013

Neuropsychopharmacol

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Recent studies have shown that post-retrieval extinction training attenuates fear and reward-related memories in both humans and rodents. This noninvasive, behavioral approach has the potential to be used in clinical settings to treat maladaptive memories that underlie several psychiatric disorders, including drug addiction. However, few studies to date have used a post-retrieval extinction approach to attenuate addiction-related memories. In the current study, we attempted to disrupt cocaine-related memories by using the post-retrieval extinction paradigm in male Sprague Dawley rats. Results revealed that starting extinction training 1 h after cocaine contextual memory was retrieved significantly attenuated cocaine-primed reinstatement of conditioned place preference (CPP) and relapse of cocaine CPP (drug-free and cocaine-primed) following 30 days of abstinence. However, animals that did not retrieve the contextual cocaine memory before extinction training, or animals that began extinction training 24 h after retrieval (outside of the reconsolidation window), demonstrated normal cocaine CPP. Conversely, animals that received additional CPP conditioning, rather than extinction training, 1 h after reactivation of cocaine memory showed enhanced cocaine CPP compared with animals that did not reactivate the cocaine memory before conditioning. These results reveal that a behavioral manipulation that takes advantage of reconsolidation and extinction of drug memories may be useful in decreasing preference for, and abuse of, cocaine.

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No erasure effect of retrieval–extinction trial on fear memory in the hippocampus-independent and dependent paradigms

Cited by 37 publications

References 13 publications

Exposure to a fearful context during periods of memory plasticity impairs extinction via hyperactivation of frontal-amygdalar circuits

Exposure to a fearful context during periods of memory plasticity impairs extinction via hyperactivation of frontal-amygdalar circuits

Potentiating mGluR5 function with a positive allosteric modulator enhances adaptive learning

Post-Retrieval Extinction Attenuates Cocaine Memories

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