Effect of Sirtuin-1 on Synaptic Plasticity in Nucleus Accumbens in a Rat Model of Heroin Addiction

Xia, Baijuan; Li, Yixin; Li, Rongrong; Dai, Yu‐Tzu; Chen, Xingqiang; Li, Jie; Wenmei, Liang

doi:10.12659/msm.910550

Cited by 11 publications

(12 citation statements)

References 34 publications

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“…Our results suggested that CUMS reduced the synaptic strength and neurotransmission efficiency in the neural circuit via decreasing the number of excitatory synapses, the postsynaptic density and increasing the width of synaptic cleft in BLA in susceptible mice. Previous studies have reported that SIRT1 regulates the transcriptional activity by regulating the histones acetylation at the promoter region of genes, such as BDNF, Syn and PSD95 46 . These changes in transcriptional activity ultimately affect the synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

Guo

Deji

Han

et al. 2021

Genes Brain and Behavior

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Previous investigations have implicated the basolateral amygdala (BLA) epigenetic mechanisms in the pathophysiology of depression. SIRT1 is a NAD+‐dependent class III histone deacetylase, widely expresses in BLA. However, epigenetic mechanisms in the BLA under the regulation of SIRT1 in the depression are largely uncharacterized. Under the chronic unpredictable chronic mild stress (CUMS) mouse model, we used adeno‐associated viral vectors (AAV) that encoded SIRT1‐shRNA or SIRT1 to specifically knockdown or overexpress SIRT1 in BLA neurons, respectively. CUMS procedure induced significant depression symptoms including the decreased sucrose preference, the less bodyweight gained, the decreased immobile latency and the increased immobile time both in forced swim test (FST) and tail suspension test (TST). Knockdown of SIRT1 in BLA glutamatergic neurons reversed these depression‐like behaviors and restored the synaptic abnormalities. Overexpression of SIRT1 in BLA glutamatergic neurons induced depression‐like behaviors in non‐stressed control mice. The result of protein expressions and ultrastructural changes were consistent with the behavioral results. Our study suggested that downregulation of SIRT1 in BLA has certain beneficial effect on CUMS‐induced depression‐like behaviors such as anorexia, anhedonia, hopelessness and despair. In addition, the increased expression of SIRT1 may be the immediate cause of depressive‐like symptoms. The abnormal expression of SIRT1 may affect the transcriptional regulation mechanism and signaling protein acetylation, affecting neuroplasticity and ultimately contribute to MDD. In the stress‐susceptible mice, these two mechanisms may co‐exist, but the specific mechanism needs further research.

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Section: Discussionmentioning

confidence: 99%

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

Guo

Deji

Han

et al. 2021

Genes Brain and Behavior

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“…SIRT1 is able to deacetylate histones as well as emerging non-histone substrates that contribute to various signaling pathways 31–33. A growing number of studies have suggested that SIRT1 serves as an essential modulator of DNA injury, inflammation, survival extension, metabolism stress, and tumor progression 34–36. In terms of inflammation, SIRT1 is able to deacetylate some transcription factors as well as modulate immune cell reactions 37.…”

Section: Discussionmentioning

confidence: 99%

<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-κB pathway</p>

Zhou¹,

Yang²,

Li³

2019

OTT

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Background Tumor-associated macrophages (TAMs) serve as crucial modulators of the complicated interaction between cancer cells and immune microenvironment. Sirtuin 1 (SIRT1) has an impact on immune reactions in cancer progression. Current knowledge of the role of SIRT1 in the regulation of M1-like macrophages as well as in hepatocellular carcinoma (HCC) is insufficient. Methods SIRT1 expression in HCC tissues was detected using quantitative reverse transcriptase PCR (qRT-PCR) and Western blot. M1 markers were detected by qRT-PCR and flow cytometry assay. Moreover, the influence of SIRT1 on HCC cell apoptosis, migration, and invasion was studied using transwell assay, flow cytometry assay, and TUNEL assays, respectively. Results In this study, it was revealed that SIRT1 was upregulated in patients suffering from HCC; these patients were also shown to have elevated levels of M1-like TAM infiltration. SIRT1 was able to reinforce M1-like macrophage infiltration and inhibit HCC metastasis. Furthermore, SIRT1 enhanced NF-κB stimulation, promoting phosphorylation of p65, IκB, and IκB kinase. It was further demonstrated in our study that SIRT1 had an impact on polarization of M1 through the NF-κB pathway. NF-κB repression downregulated M1 markers in macrophages, which excessively expressed SIRT1 and counteracted the influence of SIRT1 on migration of HCC cells. Conclusion Taken together, these results offer proof that SIRT1 is an essential regulator of the immune reaction that counteracts malignant HCC cell migration as well as growth, indicating that macrophage SIRT1 could serve as an innovative target to treat HCC.

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“…This includes miR-34a in fatty liver disease 53 , miR-195a in lipotoxic cardiomyopathy and diabetic retinopathy 54 , and miR-199a in cardiac myocyte hypoxia 55 . Specific to drug dependence, previous work has notably shown that SIRT1 is upregulated in the NAc in male mice and rats administered (IP) cocaine, morphine, or heroin 34 . Although a follow-up study by Ferguson and collegues 31 , 32 revealed that although the total number of SIRT1 binding sites is increased following 7 days of IP cocaine injections, drug administration results in depletion of SIRT1 from genic regions, specifically gene promoters.…”

Section: Discussionmentioning

confidence: 99%

“…This was validated by real time polymerase chain reaction (RT-PCR). Further, bioinformatics analysis to assess common targets of miR-199/214 identified Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)- dependent deacetylase that plays a role in apoptosis, neuron survival, stress resistance, and regulation of drug dependence 31 – 34 . Using western-blot, we confirmed expression of SIRT1 was only downregulated in the brains of nicotine exposed female rats, with no expression change in the males.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA cluster miR199a/214 are differentially expressed in female and male rats following nicotine self-administration

Pittenger

Schaal

Moore

et al. 2018

Sci Rep

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Previous research has established sex differences associated with nicotine intake, however a significant gap in knowledge remains regarding the molecular mechanisms that govern these differences at the transcriptional level. One critical regulator of transcription are microRNAs (miRNAs). miRNAs are a family of non-coding RNAs that regulate an array of important biological functions altered in several disease states, including neuroadaptive changes within the brain associated with drug dependence. We examined the prefrontal cortex (PFC) from male and female Sprague-Dawley rats following self-administration (22 days) of nicotine or yoked saline controls using next generation RNA-Sequencing (RNA-Seq) technology and found an array of miRNAs to be significantly and differentially regulated by nicotine self-administration. Of these, we found the expression of miR-199a and 214, which are expressed on the same cluster of chromosome 1, to be upregulated in the female rats exposed to nicotine; upregulation in this group was further validated by real time polymerase chain reaction (RT-PCR). Bioinformatics analysis to assess common targets of miR-199/214 identified Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)- dependent deacetylase that plays a role in apoptosis, neuron survival, and stress resistance. Using western-blot, we confirmed downregulation of SIRT1 and increased cleaved caspase 3 expression in the brains of nicotine-exposed female rats and no change in expression levels in the other groups. Collectively, our findings highlight a miR-199/214 regulatory network that, through SIRT1, may be associated with nicotine seeking in females which may serve as a potential therapeutic target for sex-specific treatment approaches.

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Effect of Sirtuin-1 on Synaptic Plasticity in Nucleus Accumbens in a Rat Model of Heroin Addiction

Cited by 11 publications

References 34 publications

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-κB pathway</p>

MicroRNA cluster miR199a/214 are differentially expressed in female and male rats following nicotine self-administration

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Effect of Sirtuin-1 on Synaptic Plasticity in Nucleus Accumbens in a Rat Model of Heroin Addiction

Cited by 11 publications

References 34 publications

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-&kappa;B pathway</p>

MicroRNA cluster miR199a/214 are differentially expressed in female and male rats following nicotine self-administration

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<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-κB pathway</p>