scholarly journals On the boundary conditions of avoidance memory reconsolidation: An attractor network perspective

2020 ◽  
Vol 127 ◽  
pp. 96-109
Author(s):  
Rodrigo M.M. Santiago ◽  
Adriano B.L. Tort
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Andressa Radiske ◽  
Maria Carolina Gonzalez ◽  
Janine I. Rossato ◽  
Gênedy Apolinário ◽  
João R. de Oliveira ◽  
...  

AbstractAvoidance memory is destabilized when recalled concurrently with conflicting information, and must undergo a hippocampus-dependent restabilization process called reconsolidation to persist. CaMKII is a serine/threonine protein kinase essential for memory processing; however, its possible involvement in avoidance memory reconsolidation has not yet been studied. Using pharmacological, electrophysiological and optogenetic tools, we found that in adult male Wistar rats hippocampal CaMKII is necessary to reconsolidate avoidance memory, but not to keep it stored while inactive, and that blocking reconsolidation via CaMKII inhibition erases learned avoidance responses.


Author(s):  
Segev Barak ◽  
Koral Goltseker

Alcohol and nicotine are widely-abused legal substances worldwide. Relapse to alcohol or tobacco seeking and consumption after abstinence is a major clinical challenge, and is often evoked by cue-induced craving. Therefore, disruption of the memory for the cue-drug association is expected to suppress relapse. Memories have been postulated to become labile shortly after their retrieval, during a “memory reconsolidation” process. Interference with the reconsolidation of drug-associated memories has been suggested as a possible strategy to reduce or even prevent cue-induced craving and relapse. Here, we surveyed the growing body of studies in animal models and in humans assessing the effectiveness of pharmacological or behavioral manipulations in reducing relapse by interfering with the reconsolidation of alcohol and nicotine/tobacco memories. Our review points to the potential of targeting the reconsolidation of these memories as a strategy to suppress relapse to alcohol drinking and tobacco smoking. However, we discuss several critical limitations and boundary conditions, which should be considered to improve the consistency and replicability in the field, and for development of an efficient reconsolidation-based relapse prevention therapy.


2016 ◽  
Vol 113 (28) ◽  
pp. E3991-E3992 ◽  
Author(s):  
Matthew P. Walker ◽  
Robert Stickgold

2021 ◽  
Vol 15 ◽  
Author(s):  
Liangpei Chen ◽  
He Yan ◽  
Yufang Wang ◽  
Ziping He ◽  
Qihao Leng ◽  
...  

Drug addiction can be seen as a disorder of maladaptive learning characterized by relapse. Therefore, disrupting drug-related memories could be an approach to improving therapies for addiction. Pioneering studies over the last two decades have revealed that consolidated memories are not static, but can be reconsolidated after retrieval, thereby providing candidate pathways for the treatment of addiction. The limbic–corticostriatal system is known to play a vital role in encoding the drug memory engram. Specific structures within this system contribute differently to the process of memory reconsolidation, making it a potential target for preventing relapse. In addition, as molecular processes are also active during memory reconsolidation, amnestic agents can be used to attenuate drug memory. In this review, we focus primarily on the brain structures involved in storing the drug memory engram, as well as the molecular processes involved in drug memory reconsolidation. Notably, we describe reports regarding boundary conditions constraining the therapeutic potential of memory reconsolidation. Furthermore, we discuss the principles that could be employed to modify stored memories. Finally, we emphasize the challenge of reconsolidation-based strategies, but end with an optimistic view on the development of reconsolidation theory for drug relapse prevention.


2020 ◽  
Author(s):  
Josue Haubrich ◽  
Matteo Bernabo ◽  
Karim Nader

ABSTRACTMemory reconsolidation is a fundamental plasticity process in the brain that allows established memories to be changed or erased. However, certain boundary conditions limit the parameters under which memories can be made plastic. Strong memories do not destabilize, for instance, although why they are resilient is mostly unknown. Here, we extend the understanding of the mechanisms implicated in reconsolidation-resistant memories by investigating the hypothesis that specific modulatory signals shape memory formation into a state that lacks lability. We find that the activation of the noradrenaline-locus coeruleus system (NOR-LC) during strong fear memory encoding increases molecular mechanisms of stability at the expense of lability in the amygdala. Preventing the NOR-LC from modulating strong fear encoding results in the formation of memories that can undergo reconsolidation within the amygdala and thus are vulnerable to post-reactivation interference. Thus, the memory strength boundary condition on reconsolidation is set at the time of encoding by the action of the NOR-LC.


2021 ◽  
Vol 15 ◽  
Author(s):  
Liangpei Chen ◽  
He Yan ◽  
Yufang Wang ◽  
Ziping He ◽  
Qihao Leng ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Hotaka Fukushima ◽  
Yue Zhang ◽  
Satoshi Kida

AbstractMemory reconsolidation is thought to maintain or enhance an original memory or add new information to the memory. Retrieved inhibitory avoidance (IA) memory is enhanced through memory reconsolidation by activating gene expression in the amygdala, medial prefrontal cortex (mPFC), and hippocampus. However, it remains unclear how these regions interact to reconsolidate/enhance IA memory. Here, we found the interactions between the amygdala and mPFC as upstream regulators of the hippocampus for IA memory reconsolidation. Pharmacological inactivation of the amygdala, mPFC, or hippocampus immediately after IA memory retrieval blocked IA memory enhancement. More importantly, inactivation of the amygdala or mPFC blocked the induction of c-Fos in the amygdala, mPFC, and hippocampus, whereas hippocampal blockade inhibited it only in the hippocampus. These observations suggest interactions between the amygdala and mPFC and they both function as upstream regulators of the hippocampus to reconsolidate IA memory. Our findings suggest circuitry mechanisms underlying IA memory enhancement through reconsolidation between the amygdala, mPFC, and hippocampus.


2017 ◽  
Vol 37 (40) ◽  
pp. 9675-9685 ◽  
Author(s):  
Andressa Radiske ◽  
Maria Carolina Gonzalez ◽  
Sergio A. Conde-Ocazionez ◽  
Anatildes Feitosa ◽  
Cristiano A. Köhler ◽  
...  

2019 ◽  
Author(s):  
Rodrigo MM Santiago ◽  
Adriano BL Tort

AbstractThe reconsolidation and extinction of aversive memories and their boundary conditions have been extensively studied. Knowing their network mechanisms may lead to the development of better strategies for the treatment of fear and anxiety-related disorders. In 2011, Osan et al. developed a computational model for exploring such phenomena based on attractor dynamics, Hebbian plasticity and synaptic degradation induced by prediction error. This model was able to explain, in a single formalism, experimental findings regarding the freezing behavior of rodents submitted to contextual fear conditioning. In 2017, through the study of inhibitory avoidance in rats, Radiske et al. showed that the previous knowledge of a context as non-aversive is a boundary condition for the reconsolidation of the shock memory subsequently experienced in that context. In the present work, by adapting the model of Osan et al. (2011) to simulate the experimental protocols of Radiske et al. (2017), we show that such boundary condition is compatible with the dynamics of an attractor network that supports synaptic labilization common to reconsolidation and extinction. Additionally, by varying parameters such as the levels of protein synthesis and degradation, we predict behavioral outcomes, and thus boundary conditions that can be tested experimentally.


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