Extinction of aversive taste memory homeostatically prevents the maintenance of in vivo insular cortex LTP: Calcineurin participation

Rivera-Olvera, Alejandro; Nelson-Mora, Janikua; Gonsebatt, María E.; Escobar, Martha L.

doi:10.1016/j.nlm.2018.04.005

Cited by 9 publications

(6 citation statements)

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“…Furthermore, homeostatic plasticity should also be considered for further research on the extinction memory field. Indeed, we have described some shared mechanisms between Hebbian and homeostatic plasticity that allow similar outcomes, such as AMPARs internalization, depotentiation or LTD. We have also presented evidence that extinction could lead to metaplastic changes (Rivera-Olvera et al, 2018). With this full view, however, we may also question whether extinction could be considered as a behavioral metaplastic process itself.…”

Section: Discussionmentioning

confidence: 92%

“…While the induction of LTP reinforces the retention of learning, the induction of LTD facilitates its extinction ( Rodríguez-Durán et al, 2017 ). More recently, we also showed that CTA extinction allows the induction but not the maintenance of LTP in the insular cortex in vivo ( Rivera-Olvera et al, 2018 ). In like manner, homeostatic plasticity triggered by optogenetic stimulation in the hippocampus altered the balance between excitation and inhibition, thus favoring the extinction expression ( Mendez et al, 2018 ).…”

Section: Mechanisms Underlying Extinction: Hebbian and Homeostatic Plasticitymentioning

confidence: 90%

“…Shaw and collaborators showed that CaN also plays an important role in the extinction of spatial memories ( Shaw et al, 2012 ). We have recently reported that after CTA extinction, the calcineurin expression is increased in the insular cortex ( Rivera-Olvera et al, 2018 ). Similarly, increases of CaN-A were observed after fear extinction ( Alvarez-Ricartes et al, 2018 ).…”

Section: The Molecular Balance: On Calcineurin Kinases and Other Phosphatasesmentioning

confidence: 99%

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Calcineurin Participation in Hebbian and Homeostatic Plasticity Associated With Extinction

Reyes-García

Escobar

2021

Front. Cell. Neurosci.

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In nature, animals need to adapt to constant changes in their environment. Learning and memory are cognitive capabilities that allow this to happen. Extinction, the reduction of a certain behavior or learning previously established, refers to a very particular and interesting type of learning that has been the basis of a series of therapies to diminish non-adaptive behaviors. In recent years, the exploration of the cellular and molecular mechanisms underlying this type of learning has received increasing attention. Hebbian plasticity (the activity-dependent modification of the strength or efficacy of synaptic transmission), and homeostatic plasticity (the homeostatic regulation of plasticity) constitute processes intimately associated with memory formation and maintenance. Particularly, long-term depression (LTD) has been proposed as the underlying mechanism of extinction, while the protein phosphatase calcineurin (CaN) has been widely related to both the extinction process and LTD. In this review, we focus on the available evidence that sustains CaN modulation of LTD and its association with extinction. Beyond the classic view, we also examine the interconnection among extinction, Hebbian and homeostatic plasticity, as well as emergent evidence of the participation of kinases and long-term potentiation (LTP) on extinction learning, highlighting the importance of the balance between kinases and phosphatases in the expression of extinction. Finally, we also integrate data that shows the association between extinction and less-studied phenomena, such as synaptic silencing and engram formation that open new perspectives in the field.

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Section: Discussionmentioning

confidence: 92%

Section: Mechanisms Underlying Extinction: Hebbian and Homeostatic Plasticitymentioning

confidence: 90%

Section: The Molecular Balance: On Calcineurin Kinases and Other Phosphatasesmentioning

confidence: 99%

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Calcineurin Participation in Hebbian and Homeostatic Plasticity Associated With Extinction

Reyes-García

Escobar

2021

Front. Cell. Neurosci.

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“…In healthy nervous tissue, CN provides an essential mechanism for bidirectional synaptic plasticity through the induction and maintenance of activity-dependent synaptic depression (Mansuy, 2003 ). In this capacity, CN is widely thought to link Ca 2+ signaling to several forms of learning and memory, including extinction learning (Baumgärtel et al, 2008 ; de la Fuente et al, 2011 ; Rivera-Olvera et al, 2018 ). However, due to its exquisite sensitivity to Ca 2+ , CN is also frequently identified as a central player in numerous deleterious or maladaptive processes arising from Ca 2+ overload and/or dysregulation (Uchino et al, 2008 ; Mukherjee and Soto, 2011 ; Reese and Taglialatela, 2011 ; Furman and Norris, 2014 ; Sompol and Norris, 2018 ).…”

Section: Cn Dysregulation In Stroke Modelsmentioning

confidence: 99%

Astrocyte Activation and the Calcineurin/NFAT Pathway in Cerebrovascular Disease

Kraner

Norris

2018

Front. Aging Neurosci.

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Calcineurin (CN) is a Ca2+/calmodulin-dependent protein phosphatase with high abundance in nervous tissue. Though enriched in neurons, CN can become strongly induced in subsets of activated astrocytes under different pathological conditions where it interacts extensively with the nuclear factor of activated T cells (NFATs). Recent work has shown that regions of small vessel damage are associated with the upregulation of a proteolized, highly active form of CN in nearby astrocytes, suggesting a link between the CN/NFAT pathway and chronic cerebrovascular disease. In this Mini Review article, we discuss CN/NFAT signaling properties in the context of vascular disease and use previous cell type-specific intervention studies in Alzheimer’s disease and traumatic brain injury models as a framework to understand how astrocytic CN/NFATs may couple vascular pathology to neurodegeneration and cognitive loss.

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“…16,17 The insular cortex (IC), which contains the gustatory cortex, plays an important role in CTA extinction. 12,18 Acute infusion of BDNF into the IC has been reported to promote CTA extinction, 19 while transient inhibition of protein synthesis with cyclosporine A in this region was found to delay CTA extinction. 20 However, the roles played by endogenous BDNF were not addressed in these studies.…”

Section: Introductionmentioning

confidence: 99%

<p>Conditioned taste aversion memory extinction temporally induces insular cortical BDNF release and inhibits neuronal apoptosis</p>

Liu

Zhang

et al. 2019

NDT

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Background: Memory extinction has been reported to be related to psychiatric disorders, such as post-traumatic stress disorder (PTSD). Secretion and synthesis of brain-derived neurotrophic factor (BDNF) have been shown to temporally regulate various memory processes via activation of tropomyosin-related kinase B (TrkB) receptors. However, whether memory extinction induces the synthesis and secretion of BDNF on the basis of its localization is not understood. In this study, we aim to investigate activity-dependent BDNF secretion and synthesis in the insular cortex (IC) in the setting of conditioned taste aversion (CTA) memory extinction. Materials and methods: Rats were subjected to CTA memory extinction and BDNF antibody (or the equal volume of vehicle) was microinjected into the IC immediately after the extinction testing. Real-time polymerase chain reaction and in situ hybridization were used to detect the gene expression of BDNF, NGF and NT4. The protein levels of BDNF were determined through the enzyme-linked immunosorbent assay. In addition, the levels of phosphorylated TrkB normalized to total TrkB were evaluated using immunoprecipitation and immunoblotting. c-Fos, total extracellular signal-regulated kinase (Erk), phosphorylated Erk, and apoptosis-related protein (caspase-3), were detected by Western blotting. Results: We found that blocking BDNF signaling within the IC disrupts CTA extinction, suggesting that BDNF signaling in the IC is necessary for CTA extinction. Increased expression levels of c-Fos indicate the induced neuronal activity in the IC during CTA extinction. In addition, temporal changes in the gene expression and protein levels of BDNF in the IC were noted during extinction. Moreover, we found that phosphorylation of TrkB increased prior to the enhanced BDNF expression, suggesting that CTA extinction induces rapid activity-dependent BDNF secretion in the IC. Finally, we found decreased expression of caspase-3 in the IC after CTA extinction. Conclusion: These results demonstrate that CTA memory extinction temporally induces the release and synthesis of BDNF in the IC and inhibits neuronal apoptosis.

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Extinction of aversive taste memory homeostatically prevents the maintenance of in vivo insular cortex LTP: Calcineurin participation

Cited by 9 publications

References 61 publications

Calcineurin Participation in Hebbian and Homeostatic Plasticity Associated With Extinction

Calcineurin Participation in Hebbian and Homeostatic Plasticity Associated With Extinction

Astrocyte Activation and the Calcineurin/NFAT Pathway in Cerebrovascular Disease

<p>Conditioned taste aversion memory extinction temporally induces insular cortical BDNF release and inhibits neuronal apoptosis</p>

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