Effect of pharmacological manipulations on Arc function

Yakout, Dina W.; Shree, Nitheyaa; Mabb, Angela M.

doi:10.1016/j.crphar.2020.100013

Cited by 8 publications

(7 citation statements)

References 144 publications

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“…Although Arc protein expression is induced in neurons by multiple stimuli [52], only a few studies showed a causal link between Arc expression and animal behavior. In particular, Arc affects memory formation, cognitive exibility, anxiety, cocaine self-administration and schizophrenia-related behaviors [22,[53][54][55][56][57].…”

Section: Discussionmentioning

confidence: 99%

Arc controls alcohol cue relapse by a central amygdala mechanism

et al. 2022

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Alcohol use disorder (AUD) is a chronic and fatal disease. The main impediment of the AUD therapy is a high probability of relapse to alcohol abuse even after prolonged abstinence. The molecular mechanisms of cue-induced relapse are not well established, despite the fact that they may offer new targets for the treatment of AUD. Using a comprehensive animal model of AUD, virally-mediated and amygdala-targeted genetic manipulations by CRISPR/Cas9 technology and ex vivo electrophysiology, we identify a mechanism that selectively controls cue-induced alcohol relapse and AUD symptom severity. This mechanism is based on activity-regulated cytoskeleton-associated protein (Arc)/ARG3.1-dependent plasticity of the amygdala synapses. In humans, we identi ed single nucleotide polymorphisms in the ARC gene and their methylation predicting not only amygdala size, but also frequency of alcohol use, even at the onset of regular consumption. Targeting Arc during alcohol cue exposure may thus be a selective new mechanism for relapse prevention.

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Section: Discussionmentioning

confidence: 99%

Arc controls alcohol cue relapse by a central amygdala mechanism

et al. 2022

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“…4A and Tables S4, S7). Arc is involved in activity-dependent neuronal plasticity in the brain [76] as well as acute and chronic neuroinflammation [77]. We found no prior reports of Arc function or expression in the retina; yet Arc's upregulation in Müller glia following KCl treatment is consistent with its role in other regions of the CNS.…”

Section: Cell Type-specific Response To Stress Injury and Disease In ...mentioning

confidence: 54%

Latent Epigenetic Programs in Müller Glia Contribute to Stress, Injury, and Disease Response in the Retina

Norrie,

Lupo,

Shirinifard

et al. 2023

Preprint

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Previous studies have demonstrated the dynamic changes in chromatin structure during retinal development that correlate with changes in gene expression. However, a major limitation of those prior studies was the lack of cellular resolution. Here, we integrate single-cell (sc) RNAseq and scATACseq with bulk retinal data sets to identify cell type specific changes in the chromatin structure during development. Although most genes promoter activity is strongly correlated with chromatin accessibility, we discovered several hundred genes that were transcriptionally silent but had accessible chromatin at their promoters. Most of those silent/accessible gene promoters were in the Muller glial cells. The Muller cells are radial glia of the retina and perform a variety of essential functions to maintain retinal homeostasis and respond to stress, injury, or disease. The silent/accessible genes in Muller glia are enriched in pathways related to inflammation, angiogenesis, and other types of cell-cell signaling and were rapidly activated when we tested 15 different physiologically relevant conditions to mimic retinal stress, injury, or disease in human and murine retinae. We refer to these as pliancy genes because they allow the Muller glia to rapidly change their gene expression and cellular state in response to different types of retinal insults. The Muller glial cell pliancy program is established during development, and we demonstrate that pliancy genes are necessary and sufficient for regulating inflammation in the murine retina in vivo. In zebrafish, Muller glia can de-differentiate and form retinal progenitor cells that replace lost neurons. The pro-inflammatory pliancy gene cascade is not activated in zebrafish Muller glia following injury, and we propose a model in which species-specific pliancy programs underly the differential response to retinal damage in species that can regenerate retinal neurons (zebrafish) versus those that cannot (humans and mice).

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“…Evidence of involvement of Arc in AD pathology and the role of Arc in regulating learning and memory which are severely disrupted in AD raises the possibility of targeting Arc therapeutically to ameliorate some of these disruptions. Several drugs are known to alter Arc levels and function, including psychotropic drugs as well as other drugs that manipulate the proteasome and the autophagy-lysosome systems, most of which are well-studied and are already in use to treat other disorders ( 103 ). However, given the complexity of the role of Arc in AD, the desired effect of pharmacologically altering Arc remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Tau regulates Arc stability in neuronal dendrites via a proteasome-sensitive but ubiquitin-independent pathway

Yakout,

Shroff,

Wei

et al. 2024

Journal of Biological Chemistry

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Effect of pharmacological manipulations on Arc function

Cited by 8 publications

References 144 publications

Arc controls alcohol cue relapse by a central amygdala mechanism

Arc controls alcohol cue relapse by a central amygdala mechanism

Latent Epigenetic Programs in Müller Glia Contribute to Stress, Injury, and Disease Response in the Retina

Tau regulates Arc stability in neuronal dendrites via a proteasome-sensitive but ubiquitin-independent pathway

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