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Kim, Juhwan,Lee, Sueun,Kang, Sohi,Jeon, Tae-Il,Kang, Man-Jong,Lee, Tae-Hoon,Kim, Yong Sik,Kim, Key-Sun,Im, Heh-In,Moon, Changjong Korean Society for Molecular and Cellular Biology 2018 Molecules and cells Vol.41 No.5
Crosstalk between G-protein signaling and glutamatergic transmission within the brain reward circuits is critical for long-term emotional effects (depression and anxiety), cravings, and negative withdrawal symptoms associated with opioid addiction. A previous study showed that Regulator of G-protein signaling 4 (RGS4) may be implicated in opiate action in the nucleus accumbens (NAc). However, the mechanism of the NAc-specific RGS4 actions that induce the behavioral responses to opiates remains largely unknown. The present study used a short hairpin RNA (shRNA)-mediated knock-down of RGS4 in the NAc of the mouse brain to investigate the relationship between the activation of ionotropic glutamate receptors and RGS4 in the NAc during morphine reward. Additionally, the shRNA-mediated RGS4 knock-down was implemented in NAc/striatal primary-cultured neurons to investigate the role that striatal neurons have in the morphine-induced activation of ionotropic glutamate receptors. The results of this study show that the NAc-specific knock-down of RGS4 significantly increased the behaviors associated with morphine and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc. Furthermore, the knock-down of RGS4 enhanced the phosphorylation of the GluR1 and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous morphine withdrawal. These findings show a novel molecular mechanism of RGS4 in glutamatergic transmission that underlies the negative symptoms associated with morphine administration.
Brain Reward Circuits in Morphine Addiction
Kim, Juhwan,Ham, Suji,Hong, Heeok,Moon, Changjong,Im, Heh-In Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.9
Morphine is the most potent analgesic for chronic pain, but its clinical use has been limited by the opiate's innate tendency to produce tolerance, severe withdrawal symptoms and rewarding properties with a high risk of relapse. To understand the addictive properties of morphine, past studies have focused on relevant molecular and cellular changes in the brain, highlighting the functional roles of reward-related brain regions. Given the accumulated findings, a recent, emerging trend in morphine research is that of examining the dynamics of neuronal interactions in brain reward circuits under the influence of morphine action. In this review, we highlight recent findings on the roles of several reward circuits involved in morphine addiction based on pharmacological, molecular and physiological evidences.
Intravenous morphine self-administration alters accumbal microRNA profiles in the mouse brain
Kim, Juhwan,Im, Heh-In,Moon, Changjong Medknow PublicationsMedia Pvt Ltd 2018 Neural regeneration research Vol.13 No.1
<P>A significant amount of evidence indicates that microRNAs (miRNAs) play an important role in drug addiction. The nucleus accumbens (NAc) is a critical part of the brain's reward circuit and is involved in a variety of psychiatric disorders, including depression, anxiety, and drug addiction. However, few studies have examined the expression of miRNAs and their functional roles in the NAc under conditions of morphine addiction. In this study, mice were intravenously infused with morphine (0.01, 0.03, 0.3, 1 and 3 mg/kg/infusion) and showed inverted U-shaped response. After morphine self-administration, NAc was used to analyze the functional networks of altered miRNAs and their putative target mRNAs in the NAc following intravenous self-administration of morphine. We utilized several bioinformatics tools, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway mapping and CyTargetLinker. We found that 62 miRNAs were altered and exhibited differential expression patterns. The putative targets were related to diverse regulatory functions, such as neurogenesis, neurodegeneration, and synaptic plasticity, as well as the pharmacological effects of morphine (receptor internalization/endocytosis). The present findings provide novel insights into the regulatory mechanisms of accumbal molecules under conditions of morphine addiction and identify several novel biomarkers associated with morphine addiction.</P>
Brain Reward Circuits in Morphine Addiction
Heh-In Im,Juhwan Kim,Suji Ham,Heeok Hong,Changjong Moon 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.9
Morphine is the most potent analgesic for chronic pain, but its clinical use has been limited by the opiate’s innate tendency to produce tolerance, severe withdrawal symp-toms and rewarding properties with a high risk of relapse. To understand the addictive properties of morphine, past studies have focused on relevant molecular and cellular changes in the brain, highlighting the functional roles of reward-related brain regions. Given the accumulated findings, a recent, emerging trend in morphine research is that of examining the dynamics of neuronal interactions in brain reward circuits under the influence of morphine action. In this review, we highlight recent findings on the roles of several reward circuits involved in morphine addiction based on pharmacological, molecular and physiological evidences.
Lee, Songhyun,Lee, Kyungho,Im, Juhwan,Kim, Hyungjun,Choi, Minkee Elsevier 2015 Journal of catalysis Vol.325 No.-
<P><B>Abstract</B></P> <P>Historically, Pt/LTA (<I>e.g</I>., Pt/NaA) has often been used as a model catalyst for studying the catalytic functions of hydrogen spillover (H spillover). Notably, none of the works reported appreciable catalytic activities for Pt/LTA alone, while markedly enhanced activities were reported after physical dilution with some acidic oxides. It was often speculated without experimental evidence that activated hydrogen generated from Pt/LTA can migrate to the diluents surface (“inter-particular” H spillover) where organic reactants can react with spilt-over hydrogen. In this work, we carefully studied benzene hydrogenation activities of Pt/NaA and its decationized form (Pt/HA), before and after the physical dilution with various metal oxides possessing different Lewis and Brønsted acidity. The originally negligible activity of Pt/NaA increased significantly after mixing with various acidic oxides. The physical dilutions, however, resulted in a significant alteration of Pt/NaA structure due to solid-state H<SUP>+</SUP> exchange, which made the catalytic interpretation vague. In contrast, Pt/HA structure did not change after the dilutions, and thus could be used as an ideal catalytic model system for studying inter-particular H spillover. The catalytic results showed that Al-rich metal oxides with abundant Lewis acid sites are effective for enhancing the catalytic activity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Catalytic effects of physically diluting Pt/NaA and Pt/HA with various acidic metal oxides were studied. </LI> <LI> Physical dilution altered the original structure of Pt/NaA due to solid-state H<SUP>+</SUP>-exchange. </LI> <LI> Physical dilution did not change the structure of decationized form of Pt/NaA (Pt/HA). </LI> <LI> Dilution with Al-rich metal oxides can markedly enhance the catalytic activity of Pt/HA. </LI> <LI> Lewis acid sites may play a significant role in the catalytic use of hydrogen spillover. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Lee, Sueun,Kang, Sohi,Ang, Mary Jasmin,Kim, Juhwan,Kim, Jong Choon,Kim, Sung‐,Ho,Jeon, Tae‐,Il,Jung, Chaeyong,Im, Seung‐,Soon,Moon, Changjong BLACKWELL 2019 GENES BRAIN AND BEHAVIOR Vol.18 No.4
<P>Schizophrenia is a hereditary disease that approximately 1% of the worldwide population develops. Many studies have investigated possible underlying genes related to schizophrenia. Recently, clinical studies suggested sterol regulatory element‐binding protein (SREBP) as a susceptibility gene in patients with schizophrenia. SREBP controls cellular lipid homeostasis by three isoforms: SREBP‐1a, SREBP‐1c and SREBP‐2. This study used SREBP‐1c knockout (KO) mice to examine whether a deficiency in SREBP‐1c would affect their emotional and psychiatric behaviors. Altered mRNA expression in genes downstream from SREBP‐1c was confirmed in the brains of SREBP‐1c KO mice. Schizophrenia‐like behavior, including hyperactivity during the dark phase, depressive‐like behavior, aggressive behavior and deficits in social interaction and prepulse inhibition, was observed in SREBP‐1c KO mice. Furthermore, increased volume of the lateral ventricle was detected in SREBP‐1c KO mice. The mRNA levels of several γ‐aminobutyric acid (GABA)‐receptor subtypes and/or glutamic acid decarboxylase 65/67 decreased in the hippocampus and medial prefrontal cortex of SREBP‐1c KO mice. Thus, SREBP‐1c deficiency may contribute to enlargement of the lateral ventricle and development of schizophrenia‐like behaviors and be associated with altered GABAergic transmission.</P>