NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1

Wang, Shaohui; Liao, Xiaomei; Liú, Dan; Hu, Juan; Yin, Yuan; Wang, Jian‐Zhi; Zhu, Ling‐Qiang

doi:10.1016/j.neuropharm.2012.06.050

Cited by 39 publications

(24 citation statements)

References 57 publications

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“…Nitrosylation did not affect the deacetylase activity of HDAC2 but rather inhibited its association with chromatin. Consistently, stimulation of PC12 cells with NGF, a plasticitypromoting neurotrophin, induced dissociation of HDAC2 from target gene promoters and enhanced histone acetylation at these same locations (78,79). A non-nitrosylatable form of HDAC2 did not dissociate from target gene promoters upon NGF treatment and prevented the increase in acetylation at these sites normally induced by NGF.…”

Section: Molecular Mechanisms Of Hdac Signalingmentioning

confidence: 72%

Histone deacetylases in memory and cognition

2014

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Over the past 30 years, lysine acetylation of histone and nonhistone proteins has become established as a key modulator of gene expression regulating numerous aspects of cell biology. Neuronal growth and plasticity are no exception; roles for lysine acetylation and deacetylation in brain function and dysfunction continue to be uncovered. Transcriptional programs coupling synaptic activity to changes in gene expression are critical to the plasticity mechanisms underlying higher brain functions. These transcriptional programs can be modulated by changes in histone acetylation, and in many cases, transcription factors and histone-modifying enzymes are recruited together to plasticity-associated genes. Lysine acetylation, catalyzed by lysine acetyltransferases (KATs), generally promotes cognitive performance, whereas the opposing process, catalyzed by histone lysine deacetylases (HDACs), appears to negatively regulate cognition in multiple brain regions. Consistently, mutation or deregulation of different KATs or HDACs contributes to neurological dysfunction and neurodegeneration. HDAC inhibitors have shown promise as a treatment to combat the cognitive decline associated with aging and neurodegenerative disease, as well as to ameliorate the symptoms of depression and posttraumatic stress disorder, among others. In this review, we discuss the evidence for the roles of HDACs in cognitive function as well as in neurological disorders and disease. In particular, we focus on HDAC2, which plays a central role in coupling lysine acetylation to synaptic plasticity and mediates many of the effects of HDAC inhibition in cognition and disease.

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Section: Molecular Mechanisms Of Hdac Signalingmentioning

confidence: 72%

Histone deacetylases in memory and cognition

2014

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“…20 Briefly, the animals were anesthetized with an intraperitoneal injection of ketamine and xylazine (85 and 15 mg/kg, respectively) and were placed on a stereotaxic instrument. The stimulating electrode was placed in the perforant path and the recording…”

Section: Electrophysiologymentioning

confidence: 99%

Resveratrol Reverses the Synaptic Plasticity Deficits in a Chronic Cerebral Hypoperfusion Rat Model

Wang

Wang³

et al. 2016

Journal of Stroke and Cerebrovascular Diseases

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“…PARylation induces a fast and transient decondensation of chromatin structure and enables the transcription needed to form long-term memory in Aplysia and mammals (18,19). It has been shown recently that PARylation is increased in the hippocampus after memory consolidation and long-term potentiation (LTP), whereas inhibition of PARylation blocked memory and LTP induction (17).…”

mentioning

confidence: 99%

Essential role of poly(ADP-ribosyl)ation in cocaine action

Scobie

Damez-Werno

Sun

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Many of the long-term effects of cocaine on the brain's reward circuitry have been shown to be mediated by alterations in gene expression. Several chromatin modifications, including histone acetylation and methylation, have been implicated in this regulation, but the effect of other histone modifications remains poorly understood. Poly(ADP-ribose) polymerase-1 (PARP-1), a ubiquitous and abundant nuclear protein, catalyzes the synthesis of a negatively charged polymer called poly(ADP-ribose) or PAR on histones and other substrate proteins and forms transcriptional regulatory complexes with several other chromatin proteins. Here, we identify an essential role for PARP-1 in cocaine-induced molecular, neural, and behavioral plasticity. Repeated cocaine administration, including self-administration, increased global levels of PARP-1 and its mark PAR in mouse nucleus accumbens (NAc), a key brain reward region. Using PARP-1 inhibitors and viral-mediated gene transfer, we established that PARP-1 induction in NAc mediates enhanced behavioral responses to cocaine, including increased self-administration of the drug. Using chromatin immunoprecipitation sequencing, we demonstrated a global, genome-wide enrichment of PARP-1 in NAc of cocaine-exposed mice and identified several PARP-1 target genes that could contribute to the lasting effects of cocaine. Specifically, we identified sidekick-1-important for synaptic connections during development-as a critical PARP-1 target gene involved in cocaine's behavioral effects as well as in its ability to induce dendritic spines on NAc neurons. These findings establish the involvement of PARP-1 and PARylation in the long-term actions of cocaine.histone PARylation | drug addiction | medium spiny neurons

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NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1

Cited by 39 publications

References 57 publications

Histone deacetylases in memory and cognition

Histone deacetylases in memory and cognition

Resveratrol Reverses the Synaptic Plasticity Deficits in a Chronic Cerebral Hypoperfusion Rat Model

Essential role of poly(ADP-ribosyl)ation in cocaine action

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