Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Yanjiong Chen is active.

Publication


Featured researches published by Yanjiong Chen.


Journal of Neuroscience Research | 2012

Distinct roles of dopamine D3 receptors in modulating methamphetamine-induced behavioral sensitization and ultrastructural plasticity in the shell of the nucleus accumbens

Jie Zhu; Yanjiong Chen; Na Zhao; Guofen Cao; Yong-hui Dang; Wei Han; Ming Xu; Teng Chen

Persistent changes in behavior and psychological function that occur as a consequence of exposure to drugs of abuse are thought to be mediated by the structural plasticity of specific neural circuits such as the brains dopamine (DA) system. Changes in dendritic morphology in the nucleus accumbens (NAc) accompany drug‐induced enduring behavioral and molecular changes, yet ultrastructural changes in synapses following repeated exposure to drugs have not been well studied. The current study examines the role of DA D3 receptors in modulating locomotor activity induced by both acute and repeated methamphetamine (METH) administration and accompanying ultrastructural plasticity in the shell of NAc in mice. We found that D3 receptor mutant (D3−/−) mice exhibited attenuated acute locomotor responses as well as the development of behavioral sensitization to METH compared with wild‐type mice. In the absence of obvious neurotoxic effects, METH induced similar increases in synaptic density in the shell of NAc in both wild‐type and D3−/− mice. These results suggest that D3 receptors modulate locomotor responses to both acute and repeated METH treatment. In contrast, the D3 receptor is not obviously involved in modulating baseline or METH‐induced ultrastructural changes in the NAc shell.


Physiology & Behavior | 2013

Roles of levo-tetrahydropalmatine in modulating methamphetamine reward behavior

Hong-Liang Su; Jie Zhu; Yanjiong Chen; Na Zhao; Wei Han; Yong-hui Dang; Ming Xu; Teng Chen

Levo-tetrahydropalmatine (l-THP), as an alkaloid purified from the traditional Chinese herbal medicine Corydalis and Stephania, has been widely used to produce many traditional Chinese herbal preparations. The effect of l-THP on methamphetamine-induced reward learning still remains unclear although it has been proved to be effective on treating allodynia and drug addiction. This experiment has been designed to examine the effect of l-THP on the acquisition, expression, extinction, and reinstatement of methamphetamine-induced conditioned place preference (CPP) in mice. The results show that methamphetamine (METH) could induce CPP in mice at doses of 0.5mg/kg, 1.0mg/kg and 2.0mg/kg respectively, but l-THP alone could not do so. Meanwhile, l-THP could not induce conditioned place aversion at doses of 1.25mg/kg to 20.0mg/kg in mice, but it could attenuate the acquisition and expression of METH-induced CPP and facilitate the extinction of METH-induced CPP in mice. Besides, l-THP could inhibit the reinstatement of METH-induced CPP at the dose of 10.0mg/kg whether it was given in the extinction training phase or 30min before the reinstatement. These results suggest that l-THP can globally suppress the rewarding properties of METH on all phases of the CPP task and it may have potential effects on the treatment of METH abuse.


BMC Neuroscience | 2015

Methamphetamine induces alterations in the long non-coding RNAs expression profile in the nucleus accumbens of the mouse

Li Zhu; Jie Zhu; Yufeng Liu; Yanjiong Chen; Yanlin Li; Liren Huang; Sisi Chen; Tao Li; Yong-hui Dang; Teng Chen

BackgroundRepeated exposure to addictive drugs elicits long-lasting cellular and molecular changes. It has been reported that the aberrant expression of long non-coding RNAs (lncRNAs) is involved in cocaine and heroin addiction, yet the expression profile of lncRNAs and their potential effects on methamphetamine (METH)-induced locomotor sensitization are largely unknown.ResultsUsing high-throughput strand-specific complementary DNA sequencing technology (ssRNA-seq), here we examined the alterations in the lncRNAs expression profile in the nucleus accumbens (NAc) of METH-sensitized mice. We found that the expression levels of 6246 known lncRNAs (6215 down-regulated, 31 up-regulated) and 8442 novel lncRNA candidates (8408 down-regulated, 34 up-regulated) were significantly altered in the METH-sensitized mice. Based on characterizations of the genomic contexts of the lncRNAs, we further showed that there were 5139 differentially expressed lncRNAs acted via cis mechanisms, including sense intronic (4295 down-regulated and one up-regulated), overlapping (25 down-regulated and one up-regulated), natural antisense transcripts (NATs, 148 down-regulated and eight up-regulated), long intergenic non-coding RNAs (lincRNAs, 582 down-regulated and five up-regulated), and bidirectional (72 down-regulated and two up-regulated). Moreover, using the program RNAplex, we identified 3994 differentially expressed lncRNAs acted via trans mechanisms. Gene ontology (GO) and KEGG pathway enrichment analyses revealed that the predicted cis- and trans- associated genes were significantly enriched during neuronal development, neuronal plasticity, learning and memory, and reward and addiction.ConclusionsTaken together, our results suggest that METH can elicit global changes in lncRNA expressions in the NAc of sensitized mice that might be involved in METH-induced locomotor sensitization and addiction.


Neuroscience Letters | 2010

Dopamine D3 receptor regulates basal but not amphetamine-induced changes in pain sensitivity in mice

Jie Zhu; Yanjiong Chen; Jianghua Lai; Yong-hui Dang; Yan Cx; Ming Xu; Teng Chen

Pain is a complex and subjective experience that involves not only the transduction of noxious stimuli by nociceptive fibers, but also the cognitive and emotional processing by the brain. Previous studies on the transmission of nociception suggest that the activation of mesolimbic dopamine (DA) system plays an important role in mediating the suppression of tonic pain. The aim of the current study was to examine the role of DA D3 receptor in modulating basal and amphetamine-induced changes in pain sensitivity in mice. We used wild-type and D3 receptor mutant mice and determined allodynia induced by both noxious heat (radiant heat) and mechanical (von Frey hair) stimuli. We show that D3 receptor mutant mice exhibit hypoalgesia in both the tail-flick test and von Frey hair test compared to wild-type mice. Amphetamine-induced hyperalgesia in both D3 receptor mutant and wild-type mice in the tail-flick test and von Frey hair test. There was no significantly difference in the relative change in pain sensitivity between wild-type and D3 receptor mutant mice in both the tail-flick test and von Frey hair test following amphetamine administration. These results suggest that the D3 receptor regulates the transmission of nociception. Moreover, amphetamine can lower pain threshold in mice.


International Journal of Molecular Medicine | 2014

PE‑induced apoptosis in SMMC‑7721 cells: Involvement of Erk and Stat signalling pathways

Li Xue; Ming Li; Teng Chen; Haifeng Sun; Jie Zhu; Xia Li; Feng Wu; Biao Wang; Juping Li; Yanjiong Chen

Emerging evidence indicates that the redistribution of phosphatidylethanolamine (PE) across the bilayer of the plasma membrane is an important molecular marker for apoptosis. However, the effect of PE on apoptosis and the underlying mechanism of PE remain unclear. In the current study, MTT and flow cytometric assays were used to examine the effects of PE on apoptosis in SMMC-7721 cells. The level of mitochondrial membrane potential (ΔΨm) and the expression of Bax, Bcl-2, caspase-3, phospho-Erk and phospho-Stat1/2 in SMMC-7721 cells that were exposed to PE were also investigated. The results showed that PE inhibited proliferation, caused G0/G1 phase cell cycle arrest and induced apoptosis in SMMC-7721 cells in a dose-dependent manner. Rhodamine 123 staining showed that the treatment of SMMC-7721 cells with different concentrations of PE for 24 h significantly decreased the level of ΔΨm and exerted dose-dependent effects. Using immunofluorescence and western blotting, we found that the expression of Bax was upregulated, whereas that of Bcl-2 was downregulated in PE-induced apoptotic cells. In addition, these events were accompanied by an increase in caspase-3 expression in a dose-dependent manner following PE treatment. PE-induced apoptosis was accompanied by a decrease in Erk phosphorylation and by the activation of Stat1/2 phosphorylation in SMMC-7721 cells. In conclusion, the results suggested that PE-induced apoptosis is involved in upregulating the Bax/Bcl-2 protein ratio and decreasing the ΔΨm. Moreover, the results showed that the Erk and Stat1/2 signalling pathways may be involved in the process of PE-induced apoptosis.


Journal of Neuroscience Research | 2015

Chronic Methamphetamine Regulates the Expression of MicroRNAs and Putative Target Genes in the Nucleus Accumbens of Mice

Li Zhu; Jie Zhu; Yufeng Liu; Yanjiong Chen; Yanlin Li; Sisi Chen; Tao Li; Yong-hui Dang; Teng Chen

MicroRNAs (miRNAs) are modulators of gene expression that play key regulatory roles in distinct cellular processes. Methamphetamine (METH) induces various aberrant changes in the limbic system by affecting a complex gene regulatory mechanism, yet the involvement of miRNAs in the effects of METH exposure remains unclear. This study identifies METH‐responsive miRNAs and their potential effects in the nucleus accumbens (NAc) of mice. Using miRNA sequencing, we examined the expression of miRNAs in the NAc of saline‐ and METH‐treated mice and identified 45 known miRNAs to be METH responsive. Additionally, we identified two novel miRNA candidates that were METH responsive (novel‐m002C and novel‐m009C). Our target prediction analysis suggested that the known METH‐regulated miRNAs might target genes that are involved in cellular autophagy, cellular metabolism, and immune responses and that the novel METH‐regulated miRNA candidates might target genes that are related to drug addiction. We also matched the predicted targets of METH‐regulated miRNAs with the NAc messenger RNA expression profile, revealing eight putative METH‐regulated target genes (Arc, Capn9, Gbp5, Lefty1, Patl2, Pde4c, Strc, and Vmn1r58). Thus, METH triggers an alteration in NAc miRNA expression, which could contribute to METH‐induced changes in neuron autophagy, metabolism, and immune responses. The differential expression of putative target genes suggests their involvement following exposure to METH.


Immunobiology | 2015

The dopamine D3 receptor regulates the effects of methamphetamine on LPS-induced cytokine production in murine mast cells.

Li Xue; Xia Li; Hui-Xun Ren; Feng Wu; Ming Li; Biao Wang; Fang-Yuan Chen; Wei-Ying Cheng; Juping Li; Yanjiong Chen; Teng Chen

Previous studies have demonstrated that methamphetamine (METH) alter inflammatory and anti-inflammatory cytokine production in the periphery. However, the effect of METH on lipopolysaccharide (LPS)-induced immune responses and its underlying mechanism of action remains unclear. The dopamine D3 receptor (D3R) plays an important role in METH addiction, indicating that the D3R may regulate METH-mediated immune responses. In this study, we examined the effect of METH on mast cell released cytokines in the lungs and thymi of mice stimulated by LPS, and on LPS-induced murine bone marrow-derived mast cells (BMMCs). Moreover, we used D3R-deficient mice to investigate the effect of this receptor on LPS-stimulated mast cell released cytokine production after METH treatment in the lungs and thymi. The effects of a D3R agonist and antagonist on LPS-induced cytokine production after METH treatment in murine BMMCs were also evaluated. METH suppressed LPS-induced cytokine production in the lungs and thymi of wild-type (WT) mice and BMMCs. However, METH did not alter LPS-induced cytokine production in the lungs and thymi of D3R-deficient mice. When BMMCs were treated with the D3R receptor antagonist, NGB2904 hydrochloride (NGB-2904), METH did not alter LPS-induced cytokine production. However, treatment with the D3R agonist, 7-hydroxy-(di-n-propylamino) tetralin (7-OH-DPAT), significantly enhanced the effects of METH on LPS-induced cytokine production. Our results suggest that METH regulates mast cell released cytokines production in an LPS-induced mouse model via the D3R.


International Immunopharmacology | 2016

The effects of D3R on TLR4 signaling involved in the regulation of METH-mediated mast cells activation

Li Xue; Yan Geng; Ming Li; Yaofeng Jin; Hui-Xun Ren; Xia Li; Feng Wu; Biao Wang; Wei-Ying Cheng; Teng Chen; Yanjiong Chen

Accumulating studies have revealed that the dopamine D3 receptor (D3R) plays an important role in methamphetamine (METH) addiction. However, the action of D3R on METH-mediated immune response and the underlying mechanism remain unclear. Mast cells (MCs) are currently identified as effector cells in many processes of immune responses, and MC activation is induced by various stimuli such as lipopolysaccharide (LPS). Moreover, CD117 and FcεRI are known as MC markers due to their specific expression in MCs. To investigate the effects of D3R on METH-mediated alteration of LPS-induced MCs activation and the underlying mechanism, in this study, we examined the expression of CD117 and FcεRI in the intestines of wild-type (D3R(+/+)) and D3R-deficient (D3R(-/-)) mice. We also measured the production of MC-derived cytokines, including TNF-α, IL-6, IL-4, IL-13 and CCL-5, in the bone marrow-derived mast cells (BMMCs) of WT and D3R(-/-) mice. Furthermore, we explored the effects of D3R on METH-mediated TLR4 and downstream MAPK and NF-κB signaling induced by LPS in mouse BMMCs. We found that METH suppressed MC activation induced by LPS in the intestines of D3R(+/)mice. In contrast, LPS-induced MC activation was less affected by METH in D3R(-/-) mice. Furthermore, METH altered LPS-induced cytokine production in BMMCs of D3R(+/+) mice but not D3R(-/-) mice. D3R was also involved in METH-mediated modulation of LPS-induced expression of TLR4 and downstream MAPK and NF-κB signaling molecules in mouse BMMCs. Taken together, our findings demonstrate that the effect of D3R on TLR4 signaling may be implicated in the regulation of METH-mediated MCs activation induced by LPS.


The International Journal of Neuropsychopharmacology | 2018

The Dopamine Receptor D3 Regulates Lipopolysaccharide-Induced Depressive-Like Behavior in Mice

Jing Wang; Yuwei Jia; Guodong Li; Biao Wang; Ting Zhou; Li Zhu; Teng Chen; Yanjiong Chen

Abstract Background The altered expression and function of dopamine receptor D3 (D3R) in patients and animal models have been correlated with depression disease severity. However, the morphological alterations and biological effects of D3R in the brain after inflammation-induced depressive-like behavior remain elusive. Methods In the present study, we ascertained the changes of D3R expression in the brain regions after depressive-like behavior induced by peripheral administration of lipopolysaccharide (LPS). Protein levels of proinflammatory cytokines, brain-derived neurotrophic factor (BDNF), and extracellular signal-regulated kinase (ERK1/2)-cAMP-response element-binding protein (CREB) signaling pathway after activation or inhibition of D3R in the brain of depressive mice were also investigated. Results LPS caused a significant reduction of D3R in the ventral tegmental area (VTA), medial prefrontal cortex (mPFC), and nucleus accumbens (NAc), which are areas related to the mesolimbic dopaminergic system. Pretreatment with pramipexole (PPX), a preferential D3R agonist, showed antidepressant effects on LPS-induced depression-like behavior through preventing changes in LPS-induced proinflammatory cytokines (tumour necrosis factor-α, interleukin-1β, and interleukin-6), BDNF, and ERK1/2-CREB signaling pathway in the VTA and NAc. In opposition, treatment with a D3R selective antagonist NGB 2904 alone made mice susceptible to depression-like effects and caused changes in accordance with the LPS-induced alterations in proinflammatory cytokines, BDNF, and the ERK1/2-CREB signaling pathway in the mPFC and NAc. Conclusions These findings provide a relevant mechanism for D3R in LPS-induced depressive-like behavior via its mediation of proinflammatory cytokines and potential cross-effects between BDNF and the ERK1/2-CREB signaling pathway.


Neuroscience Letters | 2018

Depletion of D3 dopamine receptor affects methamphetamine-induced expression patterns of Pde4b and Atf3

Yanjiong Chen; Cuo Yang; Li Zhu; Jiaqi Li; Fanglin Guan; Teng Chen

The role of the D3 dopamine receptor (D3R) and the specific molecular mechanisms underlying the regulation of D3R via the cAMP signaling pathway in methamphetamine (METH) addiction are still unclear. Here, we measured changes in Pde4b and Atf3 in the cAMP signaling pathway of dopaminergic system components, including the nucleus accumbens (NAc), caudate putamen (CPu) and hippocampus (Hip), in D3R knockout mice(D3R-/-) 1h and 24h after METH-induced behavioral sensitization. We found that knocking out D3R attenuated METH-induced behavioral sensitization, and Pde4b and Atf3 exhibited different expression patterns in brain regions in response to METH. Knocking out D3R suppressed the METH-induced increase in Pde4b in the Hip of mice 24h after the final METH injection and augmented the METH-induced increase in Atf3 in the CPu of mice 1h after the final METH injection. Our study suggests that D3R knockout controls METH-induced behavioral sensitization via regulation of Pde4b and Atf3 in different brain regions. Furthermore, the responses of Pde4b and Atf3 to METH exposure depend on the specific region of the brain involved.

Collaboration


Dive into the Yanjiong Chen's collaboration.

Top Co-Authors

Avatar

Teng Chen

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Jie Zhu

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Li Zhu

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Yong-hui Dang

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Biao Wang

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Feng Wu

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Na Zhao

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Teng Chen

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Hui-Xun Ren

Xi'an Jiaotong University

View shared research outputs
Top Co-Authors

Avatar

Juping Li

Northwest University of Politics and Law

View shared research outputs
Researchain Logo
Decentralizing Knowledge