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Metabolite signature associated with stress susceptibility in socially defeated mice
Prabhu, Vishwanath Vasudev,Nguyen, Thong Ba,Cui, Yin,Oh, Young-Eun,Piao, Yan-Hong,Baek, Hyeon-Man,Kim, Joo-Yeon,Shin, Kwang-Hee,Kim, Ji-hyun,Lee, Keon-Hak,Chung, Young-Chul Elsevier 2019 Brain Research Vol.1708 No.-
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>Social defeat represents a naturalistic form of conditioned fear and is often used as an animal model of depression. The present study aimed to identify the neurochemicals in select brain regions of mice exposed to social defeat stress.</P> <P><B>Methods</B></P> <P>Adult <I>C57BL/6N</I> mice were subjected social defeat stress for 10 days. Using high-resolution magic angle spinning <SUP>1</SUP>H nuclear magnetic resonance (HR-MAS <SUP>1</SUP>H NMR), untargeted metabolomes were measured in the amygdala (AMY), dorsal hippocampus (dHIP), dorsal striatum (dST), and prefrontal cortex (PFC).</P> <P><B>Results</B></P> <P>We observed perturbations of glutamine in the AMY; glutamate in the dHIP; glycine and myo-inositol in the dST; and aspartate, choline, and phosphoethanolamine in the PFC of susceptible and/or unsusceptible groups compared to the control group. The susceptible and unsusceptible groups significantly differed with regard to three metabolites: glutamine, glycine, and choline.</P> <P><B>Conclusion</B></P> <P>These findings suggest that social defeat stress induces disturbances in the metabolism of amino acids, lipids, and neurotransmitters in several brain areas. The resulting susceptibility-related metabolites may provide new insights into the pathophysiology underlying stress-related mental illness.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Defeated mice were classified as unsusceptible and susceptible groups. </LI> <LI> HR-MAS <SUP>1</SUP>H NMR revealed disturbances in the metabolites of defeated mice brain. </LI> <LI> Results may elucidate pathophysiological mechanisms related to stress susceptibility. </LI> </UL> </P>
Longer Telomere Length of T lymphocytes in Patients with Early and Chronic Psychosis
Yin Cui,Vishwanath Vasudev Prabhu,Thong Ba Nguyen,Subramaniam Mohana Devi,정영철 대한정신약물학회 2017 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.15 No.2
Objective: To investigate pathological conditions that act as sources of pro-inflammatory cytokines and cytotoxic substances to examine telomere length (TL) in patients with either early (duration of illness [DI] ≤5 years) or chronic (DI >5 years) psychosis using T lymphocytes. Methods: Based on these factors and the important role that T lymphocytes play in inflammation, the present study measured the TL of T lymphocytes in patients with either early or chronic psychosis. Additionally, smoking, metabolic syndrome, depression, and cognitive functioning were assessed to control for confounding effects. Results: TL was significantly longer in patients with early and chronic psychosis than in healthy control subjects and, moreover, the significance of these findings remained after controlling for age, smoking, metabolic syndrome, DI, chlorpromazine-equivalent dose, and cognitive functioning (F=9.57, degree of freedom=2, p<0.001). Additionally, the DI, chlorpromazine-equivalent doses, and the five-factor scores of the Positive and Negative Syndrome Scale were not significantly correlated with the TL of T lymphocytes in either all patients or each psychosis group. Conclusion: Possible mechanisms underlying the effects of antipsychotic medications on telomerase are discussed in the present study, but further studies measuring both telomerase activity and TL using a prospective design will be required.