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David Levitan, Yaihara Fortis-Santiago, Joshua A Figueroa, Emily E Reid, Takashi Yoshida, Nicholas C Barry, Abigail Russo, Donald B Katz
: In neuroscientists' attempts to understand the long-term storage of memory, topics of particular importance and interest are the cellular and system mechanisms of maintenance (e.g., those sensitive to ζ-inhibitory peptide, ZIP) and those induced by memory retrieval (i.e., reconsolidation). Much is known about each of these processes in isolation, but less is known concerning how they interact. It is known that ZIP sensitivity and memory retrieval share at least some molecular targets (e...
October 12, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Daniel García-Pérez, Szilamer Ferenczi, Krisztina J Kovács, M Luisa Laorden, M Victoria Milanés, Cristina Núñez
Drug-withdrawal aversive memories generate a motivational state leading to compulsive drug taking, with plasticity changes in the basolateral amygdala (BLA) being essential in aversive motivational learning. The conditioned-place aversion (CPA) paradigm allows for measuring the negative affective component of drug withdrawal. First, CPA triggers association between negative affective consequences of withdrawal with context (memory consolidation). Afterwards, when the animals are re-exposed to the paired environment, they avoid it due to the association between the context and aversive memories (memory retrieval)...
September 28, 2016: Psychoneuroendocrinology
Philipp Homan, Daniela Schiller
Long-term memories of fear have been notoriously difficult to alter. A new study finds access through the window of reconsolidation.
October 10, 2016: Current Biology: CB
R Abend, I Jalon, G Gurevitch, R Sar-El, T Shechner, D S Pine, T Hendler, Y Bar-Haim
Research associates processes of fear conditioning and extinction with treatment of anxiety and stress-related disorders. Manipulation of these processes may therefore be beneficial for such treatment. The current study examines the effects of electrical brain stimulation on fear extinction processes in healthy humans in order to assess its potential relevance for treatment enhancement. Forty-five participants underwent a 3-day fear conditioning and extinction paradigm. Electrical stimulation targeting the medial prefrontal cortex was applied during the extinction-learning phase (Day 2)...
October 11, 2016: Translational Psychiatry
Jens G Klinzing, Björn Rasch, Jan Born, Susanne Diekelmann
Sleep is known to support the consolidation of newly encoded and initially labile memories. Once consolidated, remote memories can return to a labile state upon reactivation and need to become reconsolidated in order to persist. Here we asked whether sleep also benefits the reconsolidation of remote memories after their reactivation and how reconsolidation during sleep compares to sleep-dependent consolidation processes. In three groups, participants were trained on a visuo-spatial learning task in the presence of a contextual odor...
October 6, 2016: Neurobiology of Learning and Memory
Emily Hughes, Tamila Shymansky, Hiroshi Sunada, Ken Lukowiak
Mixed results with the synthetic β-adrenergic receptor blocker, propranolol, have been reported in human populations with regards to its therapeutic efficacy for PTSD treatments targeting the memory reconsolidation process. Stress alters the ability to form and maintain memory, but whether the causal neuronal mechanisms underling memory formation in PTSD are similar to normal memory is not clear. Here, we use Lymnaea to study the effects of combinations of stressors on the quality of the formed memory state...
September 23, 2016: Neurobiology of Learning and Memory
Rie Ishikawa, Hotaka Fukushima, Paul W Frankland, Satoshi Kida
Forgetting of recent fear memory is promoted by treatment with memantine (MEM), which increases hippocampal neurogenesis. The approaches for treatment of post-traumatic stress disorder (PTSD) using rodent models have focused on the extinction and reconsolidation of recent, but not remote, memories. Here we show that, following prolonged re-exposure to the conditioning context, enhancers of hippocampal neurogenesis, including MEM, promote forgetting of remote contextual fear memory. However, these interventions are ineffective following shorter re-exposures...
2016: ELife
Ryan G Parsons, David L Walker, Michael Davis
We previously showed that a single weak fear conditioning trial, that does not produce a long-term fear memory (LTM), appeared to prime memory formation such that when a second trial followed within a circumscribed time window a robust and long-lasting fear memory was formed. We also showed that this priming effect could be blocked if we interfered with protein kinase A (PKA) signaling in the amygdala during the first conditioning trial. The goals of the current study were to determine if LTM formation after the second trial depends on PKA signaling in the amygdala and to characterize the underlying memory processes engaged during the second trial that allows for LTM formation...
September 19, 2016: Neurobiology of Learning and Memory
Roopashri Holehonnur, Aarron J Phensy, Lily J Kim, Milica Milivojevic, Dat Vuong, Delvin K Daison, Saira Alex, Michael Tiner, Lauren E Jones, Sven Kroener, Jonathan E Ploski
UNLABELLED: Reconsolidation updating is a form of memory modification in which an existing memory can become destabilized upon retrieval and subsequently be modified via protein-synthesis-dependent reconsolidation. However, not all memories appear to destabilize upon retrieval and thus are not modifiable via reconsolidation updating approaches and the neurobiological basis for this remains poorly understood. Here, we report that auditory fear memories created with 10 tone-shock pairings are resistant to retrieval-dependent memory destabilization and are associated with an increase in the synaptic GluN2A/GluN2B ratio in neurons of the basal and lateral amygdala (BLA) compared with weaker fear memories created via one or three tone-shock pairings...
September 7, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
E Lax, A Friedman, R Massart, R Barnea, L Abraham, D Cheishvili, M Zada, H Ahdoot, T Bareli, G Warhaftig, L Visochek, M Suderman, M Cohen-Armon, M Szyf, G Yadid
Reward-related memory is an important factor in cocaine seeking. One necessary signaling mechanism for long-term memory formation is the activation of poly(ADP-ribose) polymerase-1 (PARP-1), via poly(ADP-ribosyl)ation. We demonstrate herein that auto-poly(ADP-ribosyl)ation of activated PARP-1 was significantly pronounced during retrieval of cocaine-associated contextual memory, in the central amygdala (CeA) of rats expressing cocaine-conditioned place preference (CPP). Intra-CeA pharmacological and short hairpin RNA depletion of PARP-1 activity during cocaine-associated memory retrieval abolished CPP...
September 6, 2016: Molecular Psychiatry
Claudia Subic-Wrana, Leslie S Greenberg, Richard D Lane, Matthias Michal, Jörg Wiltink, Manfred E Beutel
OBJECTIVES: Affective change has been considered the hallmark of therapeutic change in psychoanalysis. Psychoanalytic writers have begun to incorporate theoretically the advanced understanding of emotional processing and transformation of the affective neurosciences. We ask if this theoretical advancement is reflected in treatment techniques addressing the processing of emotion. METHODS: We review psychoanalytic models and treatment recommendations of maladaptive affect processing in the light of a neuroscientifically informed model of achieving psychotherapeutic change by activation and reconsolidation of emotional memory...
September 2016: Zeitschrift Für Psychosomatische Medizin und Psychotherapie
Mariella Bodemeier Loayza Careaga, Carlos Eduardo Neves Girardi, Deborah Suchecki
Careaga MBL, Girardi CEN, Suchecki D. Understanding posttraumatic stress disorder through fear conditioning, extinction and reconsolidation. NEUROSCI BIOBEHAV REV -Posttraumatic stress disorder (PTSD) is a psychopathology characterized by exacerbation of fear response. A dysregulated fear response may be explained by dysfunctional learning and memory, a hypothesis that was proposed decades ago. A key component of PTSD is fear conditioning and the study of this phenomenon in laboratory has expanded the understanding of the underlying neurobiological changes in PTSD...
August 31, 2016: Neuroscience and Biobehavioral Reviews
Toon T de Beukelaar, Daniel G Woolley, Kaat Alaerts, Stephan P Swinnen, Nicole Wenderoth
Reconsolidation is observed when a consolidated stable memory is recalled, which renders it transiently labile and requires re-stabilization. Motor memory reconsolidation has previously been demonstrated using a three-day design: on day 1 the memory is encoded, on day 2 it is reactivated and experimentally manipulated, and on day 3 memory strength is tested. The aim of the current study is to determine specific boundary conditions in order to consistently degrade motor memory through reconsolidation paradigms...
2016: Frontiers in Human Neuroscience
Johannes Björkstrand, Thomas Agren, Fredrik Åhs, Andreas Frick, Elna-Marie Larsson, Olof Hjorth, Tomas Furmark, Mats Fredrikson
Memories become labile and malleable to modification when recalled [1]. Fear-conditioning experiments in both rodents and humans indicate that amygdala-localized short-term fear memories can be attenuated by disruption of their reconsolidation with extinction training soon after memory activation [2-7]. However, this may not be true for natural long-term fears. Studies in rodents indicate that although it is possible to disrupt the reconsolidation of older memories [8-11], they appear to be more resistant [1, 3, 9, 12, 13]...
October 10, 2016: Current Biology: CB
Thiago R da Silva, Reinaldo N Takahashi, Leandro J Bertoglio, Roberto Andreatini, Cristina A J Stern
The mechanisms underpinning the persistence of emotional memories are inaccurately understood. Advancing the current level of understanding with regards to this aspect is of potential translational value for the treatment of post-traumatic stress disorder (PTSD), which stems from an abnormal aversive memory formation. Tamoxifen (TMX) is a drug used in chemotherapy for breast cancer and associated with poor cognitive performances. The present study investigated whether the systemic administration of TMX (1.0-50mg/kg) during and/or beyond the reconsolidation time-window could attenuate a reactivated contextual fear memory in laboratory animals...
October 2016: European Neuropsychopharmacology: the Journal of the European College of Neuropsychopharmacology
M I Zaichenko, V A Markevich, G A Grigoryan
In the current paper there were used two methods for assessment of the propranolol effect on reactivated memory at reconsolidation phase--a classical pavlovian conditioning and the two-ways escape reflex. The difference between these two models was that in the first case a tone was paired with electrocutaneous painful stimulation only once, while in the second case it was applied multiply. Reminding was produced in the first case by placing the animals into the same context, whereas in the second case by application of the same amount of pairings of conditional and unconditional stimuli as it was used at the first day of learning...
March 2016: Zhurnal Vyssheĭ Nervnoĭ Deiatelnosti Imeni I P Pavlova
N I Dubrovina
GABA is the major inhibitory neurotransmitter in the central nervous system determining the efficacy of neuronal interaction. GABA-receptors play a key role in different aspects of fear memory--acquisition and consolidation, retention, reconsolidation and extinction. Extinction is an important behavioural phenomenon which allows organism to adapt its behavior to a changing environment. Extinction of fear memory is a form of new inhibitory learning which interferes with expression of the initial acquired fear conditioning...
March 2016: Zhurnal Vyssheĭ Nervnoĭ Deiatelnosti Imeni I P Pavlova
Janine Thome, Georgia Koppe, Sophie Hauschild, Lisa Liebke, Christian Schmahl, Stefanie Lis, Martin Bohus
BACKGROUND: Dysfunctional fear responses play a central role in many mental disorders. New insights in learning and memory suggest that pharmacological and behavioural interventions during the reconsolidation of reactivated fear memories may increase the efficacy of therapeutic interventions. It has been proposed that interventions applied during reconsolidation may modify the original fear memory, and thus prevent the spontaneous recovery and reinstatement of the fear response. METHODS: We investigated whether pharmacological (propranolol) and behavioural (reappraisal, multisensory stimulation) interventions reduce fear memory, and prevent reinstatement of fear in comparison to a placebo control group...
2016: PloS One
Merel Kindt, Arnold van Emmerik
The discovery that fear memories may change upon retrieval, a process referred to as memory reconsolidation, opened avenues to develop a revolutionary new treatment for emotional memory disorders. Reconsolidation is a two-phase process in which retrieval of a memory initiates a transient period of memory destabilization, followed by a protein synthesis-dependent restabilization phase. This reconsolidation window offers unique opportunities for amnesic agents to interfere with the process of memory restabilization, thereby weakening or even erasing the emotional expression from specific fear memories...
August 2016: Therapeutic Advances in Psychopharmacology
Yang-Jung Yu, Chien-Hsuan Huang, Chih-Hua Chang, Po-Wu Gean
Destabilization refers to a memory that becomes unstable when reactivated and is susceptible to disruption by amnestic agents. Here we delineated the cellular mechanism underlying the destabilization of drug memory. Mice were conditioned with methamphetamine (MeAM) for 3 d, and drug memory was assessed with a conditioned place preference (CPP) protocol. Anisomycin (ANI) was administered 60 min after the CPP retrieval to disrupt reconsolidation. We found that destabilization of MeAM CPP after the application of ANI was blocked by the N-methyl-d-aspartate receptor (NMDAR) antagonist MK-801 and the NR2B antagonist ifenprodil (IFN) but not by the NR2A antagonist NVP-AAM077 (NVP)...
September 2016: Learning & Memory
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