On the Involvement of BDNF Signaling in Memory Reconsolidation

Gonzalez, María Carolina; Radiske, Andressa; Cammarota, Martı́n

doi:10.3389/fncel.2019.00383

Cited by 39 publications

(25 citation statements)

References 83 publications

(102 reference statements)

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“…The inability to update the original object location memory is likely due to impairments in synaptic plasticity that would prevent incorporation of new information during the update session. Previous reports observe that synaptic reactivation, which takes place when retrieval and novelty detection occur concomitantly (such is the case during the update session), re-sensitizes LTP to protein synthesis inhibition (Fonseca et al, 2006) allowing for restabilization mechanisms through a protein synthesis-dependent reconsolidation process (Gonzalez et al, 2019)). This possibility falls in line with our observed impairments in protein synthesis-dependent hippocampal LTP in male mice irradiated using 30 cGy of mixed-ion GCR (Fig.…”

Section: Discussionmentioning

confidence: 99%

Systemic HDAC3 inhibition ameliorates impairments in synaptic plasticity caused by simulated galactic cosmic radiation exposure in male mice

Keiser

Kramar

Dong

et al. 2021

Neurobiology of Learning and Memory

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Deep space travel presents a number of measurable risks including exposure to a spectrum of radiations of varying qualities, termed galactic cosmic radiation (GCR) that are capable of penetrating the spacecraft, traversing through the body and impacting brain function. Using rodents, studies have reported that exposure to simulated GCR leads to cognitive impairments associated with changes in hippocampus function that can persist as long as one-year post exposure with no sign of recovery. Whether memory can be updated to incorporate new information in mice exposed to GCR is unknown. Further, mechanisms underlying long lasting impairments in cognitive function as a result of GCR exposure have yet to be defined. Here, we examined whether whole body exposure to simulated GCR using 6 ions and doses of 5 or 30 cGy interfered with the ability to update an existing memory or impact hippocampal synaptic plasticity, a cellular mechanism believed to underlie memory processes, by examining long term potentiation (LTP) in acute hippocampal slices from middle aged male mice 3.5-5 months after radiation exposure. Using a modified version of the hippocampus-dependent object location memory task developed by our lab termed "Objects in Updated Locations" (OUL) task we find that GCR exposure impaired hippocampus-dependent memory updating and hippocampal LTP 3.5-5 months after exposure. Further, we find that impairments in LTP are reversed through one-time systemic subcutaneous injection of the histone deacetylase 3 inhibitor RGFP 966 (10 mg/kg), suggesting that long lasting impairments in cognitive function may be mediated at least in part, through epigenetic mechanisms.

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Section: Discussionmentioning

confidence: 99%

Systemic HDAC3 inhibition ameliorates impairments in synaptic plasticity caused by simulated galactic cosmic radiation exposure in male mice

Keiser

Kramar

Dong

et al. 2021

Neurobiology of Learning and Memory

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“…BDNF is a protein synthesized in the brain that offers resistance to neurodegenerative diseases and favors stress adaptation and resilience (Taliaz et al 2011; Notaras and van den Buuse 2020), but also energy homeostasis (Marosi and Mattson 2013). BDNF has emerged as one of the most important molecule in memory (Beckinschtein et al 2014; Gonzalez et al 2019). It consolidates both the within- and between-generation fear memory owing to epigenetic regulation (Lubin et al 2008; Coley et al 2019).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide epigenomic stress response in the European sea bass (Dicentrarchus labrax, L.)

Krick

Desmarais

Σαμαράς

et al. 2020

Preprint

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AbstractUnderstanding the molecular basis of stress is of long standing interest in biology and fish science. We tackled this question by modifying the epiGBS (epiGenotyping By sequencing) technique to screen for cytosine methylation and explore the genome-wide epigenomic response to a repeated acute stress challenge in the European sea bass (Dicentrarchus labrax). Following a minimally invasive sampling using nucleated red blood cells (RBCs), our modified epiGBS protocol retrieved 501,108,033 sequencing reads after trimming, with a mean mapping efficiency of 73.0% (unique best hits). Sequencing reads mapped across all linkage groups (LGs). A total of 47,983 CpG coordinates with a minimum 30X read depth was retained for differential methylation analysis between pre- and post-stress fish. A family effect was demonstrated, and 57 distinct differentially methylated cytosines (DMCs) distributed on 17 of 24 LGs were found between RBCs of pre- and post-stress individuals and located close to 51 distinct stress-related genes. Thirty-eight of these genes were previously reported as differentially expressed in the brain of zebrafish, most of them involved in stress coping differences. Some DMC-related genes appear as good candidates to study the stress response, especially a set of them associated to the Brain Derived Neurotrophic Factor (BDNF), a protein that favors stress adaptation and fear memory. Limits to our study and future directions are presented, including the use of RBCs as a surrogate to other target tissues, to provide with classical physiological measurements a more complete picture of the stress response in fish.

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“…In addition, primary hippocampal neurons exposed to ketone metabolite β-hydroxybutyrate (BHBA) brought about an upregulation of H3K27 acetylation at Bdnf promoters and also a decrease in H3K27 trimethylation, ultimately activating Bdnf transcription [ 104 ]. Brain-derived neurotrophic factor (BDNF) is one of the key regulators of synaptic plasticity and memory formation [ 105 ], and the ability of histones to regulate Bdnf transcription highlights their influence on memory and synaptic plasticity.…”

Section: Epigenetic Regulation Of Hippocampal Principal Neuronsmentioning

confidence: 99%

Epigenetic Regulation of the Hippocampus, with Special Reference to Radiation Exposure

Saw

Tang

2020

IJMS

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The hippocampus is crucial in learning, memory and emotion processing, and is involved in the development of different neurological and neuropsychological disorders. Several epigenetic factors, including DNA methylation, histone modifications and non-coding RNAs, have been shown to regulate the development and function of the hippocampus, and the alteration of epigenetic regulation may play important roles in the development of neurocognitive and neurodegenerative diseases. This review summarizes the epigenetic modifications of various cell types and processes within the hippocampus and their resulting effects on cognition, memory and overall hippocampal function. In addition, the effects of exposure to radiation that may induce a myriad of epigenetic changes in the hippocampus are reviewed. By assessing and evaluating the current literature, we hope to prompt a more thorough understanding of the molecular mechanisms that underlie radiation-induced epigenetic changes, an area which can be further explored.

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On the Involvement of BDNF Signaling in Memory Reconsolidation

Cited by 39 publications

References 83 publications

Systemic HDAC3 inhibition ameliorates impairments in synaptic plasticity caused by simulated galactic cosmic radiation exposure in male mice

Systemic HDAC3 inhibition ameliorates impairments in synaptic plasticity caused by simulated galactic cosmic radiation exposure in male mice

Genome-wide epigenomic stress response in the European sea bass (Dicentrarchus labrax, L.)

Epigenetic Regulation of the Hippocampus, with Special Reference to Radiation Exposure

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