Behavioral tagging: A novel model for studying long-term memory

Vishnoi, Shruti; Raisuddin, Sheikh; Parvez, Suhel

doi:10.1016/j.neubiorev.2016.05.017

Cited by 29 publications

(22 citation statements)

References 99 publications

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“…It is also worth noting the remarkable similarity between this time window and that observed in rodents during the behavioral tagging studies that inspired this research (Ballarini et al, 2009). In that sense, different laboratories have demonstrated that novelty is able to promote the formation of otherwise inexistent LTMs when it is experienced within a critical time window comprising the hour around training, but excluding time points beyond 2 h and immediately before or after the learning session (Redondo and Morris, 2011;Moncada et al, 2014;Vishnoi et al, 2016). Thus, the whole body of evidence suggests that the 1-h interval before or after learning is ideal to associate novel experiences to enhance the memory of content recently learned in the classroom.…”

Section: Discussionmentioning

confidence: 72%

Novelty Improves the Formation and Persistence of Memory in a Naturalistic School Scenario

et al. 2020

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Section: Discussionmentioning

confidence: 72%

Novelty Improves the Formation and Persistence of Memory in a Naturalistic School Scenario

et al. 2020

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“…The novelty-extinction was developed based on the concept of 'behavioral tagging', which evolved from the concept of 'synaptic tagging and capture'. The detailed interpretation of these hypotheses can be found here (Redondo & Morris, 2011;Moncada et al, 2015;Vishnoi et al, 2016). In this section, we will only discuss whether and how the 'novelty-extinction' protocol could benefit the treatment of drug addiction.…”

Section: Other Behavioral Modulationsmentioning

confidence: 99%

Modulating reconsolidation and extinction to regulate drug reward memory

Liu

Tian

2018

Eur J of Neuroscience

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Drug addiction is an aberrant memory that shares the same memory processes as other memories. Brief exposure to drug-associated cues could result in reconsolidation, a hypothetical process during which original memory could be updated. In contrast, longer exposure times to drug-associated cues could trigger extinction, a process that decreases the conditioned responding. In this review, we discuss the pharmacological and non-pharmacological manipulations on the reconsolidation and extinction that could be used to interfere with drug reward memories. Pharmacological agents such as β-adrenergic receptor antagonist propranolol can interfere with reconsolidation to disrupt drug reward memory. Pharmacological agents such as the NMDA receptor glycine site agonists d-cycloserine and d-serine can facilitate extinction and then attenuate the expression of drug reward memory. Besides pharmacological interventions, drug-free behavioral approaches by utilizing the reconsolidation and extinction, such as 'post-retrieval extinction' and 'UCS-retrieval extinction', are also effective to erase or inhibit the recall of drug reward memory. Taken together, pharmacological modulation and non-pharmacological modulation of reconsolidation and extinction are promising approaches to regulate drug reward memory and prevent relapse.

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“…The principle that a strong event can facilitate the persistence of a weak memory has also been demonstrated behaviorally. The process of facilitating memory persistence using a second behavioral event that provides the required protein synthesis has been called behavioral tagging ( Moncada et al, 2015 ; Redondo and Morris, 2011 ; Vishnoi et al, 2016 ; Wang and Morris, 2010 ). For example, it has been shown in inhibitory avoidance, a short-term memory can last for a long time when exploration in a novel open field occurs shortly before or after the avoidance learning ( Moncada and Viola, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

Novelty enhances memory persistence and remediates propranolol-induced deficit via reconsolidation

Wang

2018

Neuropharmacology

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Memory reactivation has been shown to open a time window for memory modulation. The majority of the methodological or pharmacological approaches target disruption of reconsolidation to weaken aversive memories. However, methods to improve appetitive memory persistence through reconsolidation or to reverse drug-induced reconsolidation impairment are limited. To improve memory persistence, previous studies show that a novel event, introduced around the time of memory encoding, enables the persistence of an otherwise decayed memory. This is mainly through a memory consolidation process. The current study first investigated if a novel event introduced during memory reactivation improves memory persistence through reconsolidation. Using a rodent appetitive spatial paradigm, similar to the human everyday experience of recalling where an item is located, a novel event around memory reactivation facilitated the persistence of spatial memory. This facilitation did not occur when the novel event was omitted and the protein synthesis-dependent reconsolidation was not affected by zif268 anti-sense in the dorsal hippocampus. Furthermore, beta-adrenergic antagonists, propranolol, impaired reconsolidation of appetitive spatial memory and contextual fear conditioning. A novel event after memory reactivation could reverse this impairment due to propranolol. Together, this study provides methods and confirmation for improving memory persistence during memory reactivation and reconsolidation.

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Behavioral tagging: A novel model for studying long-term memory

Cited by 29 publications

References 99 publications

Novelty Improves the Formation and Persistence of Memory in a Naturalistic School Scenario

Novelty Improves the Formation and Persistence of Memory in a Naturalistic School Scenario

Modulating reconsolidation and extinction to regulate drug reward memory

Novelty enhances memory persistence and remediates propranolol-induced deficit via reconsolidation

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