Modifications to cytoskeleton-associated proteins in dendritic spines underlie the adaptive plasticity involved in long term reference memory

González-Tapia, David; González-Tapia, Diana C.; Vázquez-Hernández, Nallely; Martínez-Torres, Nestor I.; Flores-Soto, M.E.; González-Burgos, Ignacio

doi:10.1016/j.nlm.2020.107247

Cited by 3 publications

(3 citation statements)

References 49 publications

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“…The ability of cofilin to accumulate with actin in the cell nucleus as rod-shaped bundles of ~10 nm filaments was first observed in cultured cells stressed by treatment with 10% DMSO or by heat shock [223]. Rods immunostain for actin but do not stain with fluorescent phalloidin, demonstrating that they do not contain "typical" F-actin.…”

Section: Cofilin Organelle Localization and Functional Consequences 71 Nucleusmentioning

confidence: 99%

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Cofilin and Actin Dynamics: Multiple Modes of Regulation and Their Impacts in Neuronal Development and Degeneration

Bamburg

Minamide

Wiggan

et al. 2021

Cells

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Proteins of the actin depolymerizing factor (ADF)/cofilin family are ubiquitous among eukaryotes and are essential regulators of actin dynamics and function. Mammalian neurons express cofilin-1 as the major isoform, but ADF and cofilin-2 are also expressed. All isoforms bind preferentially and cooperatively along ADP-subunits in F-actin, affecting the filament helical rotation, and when either alone or when enhanced by other proteins, promotes filament severing and subunit turnover. Although self-regulating cofilin-mediated actin dynamics can drive motility without post-translational regulation, cells utilize many mechanisms to locally control cofilin, including cooperation/competition with other proteins. Newly identified post-translational modifications function with or are independent from the well-established phosphorylation of serine 3 and provide unexplored avenues for isoform specific regulation. Cofilin modulates actin transport and function in the nucleus as well as actin organization associated with mitochondrial fission and mitophagy. Under neuronal stress conditions, cofilin-saturated F-actin fragments can undergo oxidative cross-linking and bundle together to form cofilin-actin rods. Rods form in abundance within neurons around brain ischemic lesions and can be rapidly induced in neurites of most hippocampal and cortical neurons through energy depletion or glutamate-induced excitotoxicity. In ~20% of rodent hippocampal neurons, rods form more slowly in a receptor-mediated process triggered by factors intimately connected to disease-related dementias, e.g., amyloid-β in Alzheimer’s disease. This rod-inducing pathway requires a cellular prion protein, NADPH oxidase, and G-protein coupled receptors, e.g., CXCR4 and CCR5. Here, we will review many aspects of cofilin regulation and its contribution to synaptic loss and pathology of neurodegenerative diseases.

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Section: Cofilin Organelle Localization and Functional Consequences 71 Nucleusmentioning

confidence: 99%

“…Additional residues comprising a bipartite NLS have since been identified [226] (Figure 4). All three ADF/cofilin isoforms have been identified in nuclear rods from different cell types [223,227,228].…”

Section: Cofilin Organelle Localization and Functional Consequences 71 Nucleusmentioning

confidence: 99%

Cofilin and Actin Dynamics: Multiple Modes of Regulation and Their Impacts in Neuronal Development and Degeneration

Bamburg

Minamide

Wiggan

et al. 2021

Cells

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“…Spine structure Dendritic spines play an indispensable role in learning and memory; and their shape, distribution, and density positively correlate with increased input (Yang et al, 2014;González-Tapia et al, 2020). The molecular composition of dendritic spines is a veritable cytoplasmic circus, with a broad array of players acting in precise spatial and temporal coordination (Murakoshi and Yasuda, 2012).…”

Section: Dendritic Spine Dynamics and Neuronal Plasticitymentioning

confidence: 99%

Sculpting Dendritic Spines during Initiation and Maintenance of Neuropathic Pain

Stratton

Khanna

2020

J. Neurosci.

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Accumulating evidence has established a firm role for synaptic plasticity in the pathogenesis of neuropathic pain. Recent advances have highlighted the importance of dendritic spine remodeling in driving synaptic plasticity within the CNS. Identifying the molecular players underlying neuropathic pain induced structural and functional maladaptation is therefore critical to understanding its pathophysiology. This process of dynamic reorganization happens in unique phases that have diverse pathologic underpinnings in the initiation and maintenance of neuropathic pain. Recent evidence suggests that pharmacological targeting of specific proteins during distinct phases of neuropathic pain development produces enhanced antinociception. These findings outline a potential new paradigm for targeted treatment and the development of novel therapies for neuropathic pain. We present a concise review of the role of dendritic spines in neuropathic pain and outline the potential for modulation of spine dynamics by targeting two proteins, srGAP3 and Rac1, critically involved in the regulation of the actin cytoskeleton.

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Plastic changes to dendritic spines in the cerebellar and prefrontal cortices underlie the decline in motor coordination and working memory during successful aging

Vázquez-Hernández

Martínez-Torres

González-Burgos

2021

Behavioural Brain Research

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Modifications to cytoskeleton-associated proteins in dendritic spines underlie the adaptive plasticity involved in long term reference memory

Cited by 3 publications

References 49 publications

Cofilin and Actin Dynamics: Multiple Modes of Regulation and Their Impacts in Neuronal Development and Degeneration

Cofilin and Actin Dynamics: Multiple Modes of Regulation and Their Impacts in Neuronal Development and Degeneration

Sculpting Dendritic Spines during Initiation and Maintenance of Neuropathic Pain

Plastic changes to dendritic spines in the cerebellar and prefrontal cortices underlie the decline in motor coordination and working memory during successful aging

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