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Gary Gilmour - One of the best experts on this subject based on the ideXlab platform.
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The group II metabotropic glutamate receptor agonist LY354740 and the D2 receptor antagonist haloperidol reduce locomotor hyperactivity but fail to rescue spatial working Memory in GluA1 knockout mice.
The European journal of neuroscience, 2017Co-Authors: Thomas Boerner, Rolf Sprengel, Peter H. Seeburg, Paul J Harrison, Alexei M. Bygrave, Jingkai Chen, Anushka Fernando, Stephanie Jackson, Chris Barkus, Gary GilmourAbstract:Group II metabotropic glutamate receptor agonists have been suggested as potential anti-psychotics, at least in part, based on the observation that the agonist LY354740 appeared to rescue the cognitive Deficits caused by non-competitive N-methyl-d-aspartate receptor (NMDAR) antagonists, including spatial working Memory Deficits in rodents. Here, we tested the ability of LY354740 to rescue spatial working Memory performance in mice that lack the GluA1 subunit of the AMPA glutamate receptor, encoded by Gria1, a gene recently implicated in schizophrenia by genome-wide association studies. We found that LY354740 failed to rescue the spatial working Memory Deficit in Gria1-/- mice during rewarded alternation performance in the T-maze. In contrast, LY354740 did reduce the locomotor hyperactivity in these animals to a level that was similar to controls. A similar pattern was found with the dopamine receptor antagonist haloperidol, with no amelioration of the spatial working Memory Deficit in Gria1-/- mice, even though the same dose of haloperidol reduced their locomotor hyperactivity. These results with LY354740 contrast with the rescue of spatial working Memory in models of glutamatergic hypofunction using non-competitive NMDAR antagonists. Future studies should determine whether group II mGluR agonists can rescue spatial working Memory Deficits with other NMDAR manipulations, including genetic models and other pharmacological manipulations of NMDAR function.
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Dataset for: The group II metabotropic glutamate receptor agonist LY354740 and the D2 receptor antagonist haloperidol reduce locomotor hyperactivity but fail to rescue spatial working Memory in GluA1 knockout mice
2017Co-Authors: Thomas Boerner, Rolf Sprengel, Peter H. Seeburg, Paul J Harrison, Alexei M. Bygrave, Jingkai Chen, Anushka Fernando, Stephanie Jackson, Chris Barkus, Gary GilmourAbstract:Group II metabotropic glutamate receptor agonists have been suggested as potential anti-psychotics, at least in part, based on the observation that the agonist LY354740 appeared to rescue the cognitive Deficits caused by non-competitive N-methyl-D-aspartate receptor (NMDAR) antagonists, including spatial working Memory Deficits in rodents. Here, we tested the ability of LY354740 to rescue spatial working Memory performance in mice that lack the GluA1 subunit of the AMPA glutamate receptor, encoded by Gria1, a gene recently implicated in schizophrenia by genome-wide association studies. We found that LY354740 failed to rescue the spatial working Memory Deficit in Gria1-/- mice during rewarded alternation performance in the T-maze. In contrast, LY354740 did reduce the locomotor hyperactivity in these animals to a level that was similar to controls. A similar pattern was found with the dopamine receptor antagonist haloperidol, with no amelioration of the spatial working Memory Deficit in Gria1-/- mice, even though the same dose of haloperidol reduced their locomotor hyperactivity. These results with LY354740 contrast with the rescue of spatial working Memory in models of glutamatergic hypofunction using non-competitive NMDAR antagonists. Future studies should determine whether group II mGluR agonists can rescue spatial working Memory Deficits with other NMDAR manipulations, including genetic models and other pharmacological manipulations of NMDAR function
Donghyun Kim - One of the best experts on this subject based on the ideXlab platform.
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probiotic mixture kf attenuates age dependent Memory Deficit and lipidemia in fischer 344 rats
Journal of Microbiology and Biotechnology, 2015Co-Authors: Jinju Jeong, Kyungah Kim, Youngtae Ahn, Jaehun Sim, Jaeyeon Woo, Chulsung Huh, Donghyun KimAbstract:To investigate the Memory-enhancing effect of lactic acid bacteria, we selected the probiotic mixture KF, which consisted of Lactobacillus plantarum KY1032 and Lactobacillus curvatus HY7601 (1 × 10(11) CFU/g of each strain), and investigated its antilipidemic and Memoryenhancing effects in aged Fischer 344 rats. KF (1 × 10(10) CFU/rat/day), which was administered orally once a day (6 days per week) for 8 weeks, significantly inhibited age-dependent increases of blood triglyceride and reductions of HDL cholesterol (p < 0.05). KF restored agereduced spontaneous alternation in the Y-maze task to 94.4% of that seen in young rats (p < 0.05). KF treatment slightly, but not significantly, shortened the escape latency daily for 4 days. Oral administration of KF restored age-suppressed doublecortin and brain-derived neurotrophic factor expression in aged rats. Orally administered KF suppressed the expression of p16, p53, and cyclooxygenase-2, the phosphorylation of Akt and mTOR, and the activation of NF-κB in the hippocampus of the brain. These findings suggest that KF may ameliorate age-dependent Memory Deficit and lipidemia by inhibiting NF-κB activation.
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ginsenosides rg5 and rh3 protect scopolamine induced Memory Deficits in mice
Journal of Ethnopharmacology, 2013Co-Authors: Eunjin Kim, Ilhoon Jung, Thi Kim Van Le, Jinju Jeong, Namjae Kim, Donghyun KimAbstract:Abstract Ethnopharmacological relevance Panax ginseng (family Araliaceae) is traditionally used as a remedy for cancer, inflammation, stress and aging. Aim of study To explore whether ginsenosides Rg5 and Rh3, the main constituents of heat-processed ginseng (the root of Panax ginseng ), could protect Memory Deficit. Materials and methods We isolated ginsenosides Rh3 and Rg5 from heated-processed ginseng treated with and without human feces, respectively. Then we investigated their protective effects on Memory impairment using the passive avoidance, Y-maze and Morris water maze tasks in mice. Memory Deficit was induced in mice by the intraperitoneal injection of scopolamine. Results Ginsenosides Rg5 or Rh3 increased the latency time reduced by scopolamine in passive avoidance test. Treatment with ginsenoside Rg5 or Rh3 significantly reversed the lowered spontaneous alteration induced by scopolamine in Y-maze task. Ginsenoisde Rg5 or Rh3 (10 mg/kg) significantly shortened the escape latencies prolonged by treatment with scopolamine on the last day of training trial sessions in Morris water maze task. Furthermore, ginsenosides Rg5 and Rh3 inhibited acetylcholinesterase activity in a dose-dependent manner, with IC 50 values of 18.4 and 10.2 μM, respectively. The inhibitory potency of ginsenoside Rh3 is comparable with that of donepezil (IC 50 =9.9 μM). These ginsenosides also reversed hippocampal brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation reduced by scopolamine. Of them, ginsenoside Rh3 more potently protected Memory Deficit. Conclusions Ginsenoside Rg5 and its metabolite ginsenoside Rh3 may protect Memory Deficit by inhibiting AChE activity and increasing BDNF expression and CREB activation.
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lactobacillus pentosus var plantarum c29 protects scopolamine induced Memory Deficit in mice
Journal of Applied Microbiology, 2012Co-Authors: Ilhoon Jung, M A Jung, Eui Jong Kim, Myung Joo Han, Donghyun KimAbstract:Aims In the preliminary study, kimchi, a traditional food fermented with Chinese cabbage, protected scopolamine-induced mouse Memory Deficit in passive avoidance test. Therefore, we screened protective ingredients, particularly lactic acid bacteria, from Chinese cabbage kimchi against scopolamine-induced Memory Deficit in mice. Methods and Results Lactic acid bacteria, isolated from Chinese cabbage kimchi, were identified by 16S rDNA sequence analysis, G+C content and cellular fatty acid composition and sugar fermentation test. Memory Deficit was induced in mice by intraperitoneally injecting with scopolamine. Kimchi, particularly its supernatant, protected scopolamine-induced Memory Deficit in mice in passive avoidance test. Of kimchi ingredients, a lactic acid bacterium, strain C29, potently protected scopolamine-induced Memory Deficit in mice. C29 was a gram-positive, catalase-negative, anaerobic and non-motile rod. Its pylogenetic property was near to Lactobacillus pentosus (99%) and Lact. plantarum (99%). However, C29 fermented inulin and L-rhamnose and grew in pH 3 and at 45°C in contrast with Lact. pentosus and Lact. plantarum. Therefore, it named to be Lact pentosus var. plantarum C29. The strain C29 protected scopolamine-induced Memory Deficit in Y-maze and Morris water maze tests. Furthermore, C29 increased hippocampal BDNF and p-CREB expressions, which were reduced by scopolamine. Conclusion Lactobacillus pentosus var. plantarum C29 may protect Memory Deficit by inducing BDNF and p-CREB expressions. Significance and Impact of the Study Lactic acid bacteria, such as Lact pentosus var. plantarum C29, may prevent Memory Deficit and its contained fermented foods may be beneficial for dementia.
Thomas Boerner - One of the best experts on this subject based on the ideXlab platform.
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The group II metabotropic glutamate receptor agonist LY354740 and the D2 receptor antagonist haloperidol reduce locomotor hyperactivity but fail to rescue spatial working Memory in GluA1 knockout mice.
The European journal of neuroscience, 2017Co-Authors: Thomas Boerner, Rolf Sprengel, Peter H. Seeburg, Paul J Harrison, Alexei M. Bygrave, Jingkai Chen, Anushka Fernando, Stephanie Jackson, Chris Barkus, Gary GilmourAbstract:Group II metabotropic glutamate receptor agonists have been suggested as potential anti-psychotics, at least in part, based on the observation that the agonist LY354740 appeared to rescue the cognitive Deficits caused by non-competitive N-methyl-d-aspartate receptor (NMDAR) antagonists, including spatial working Memory Deficits in rodents. Here, we tested the ability of LY354740 to rescue spatial working Memory performance in mice that lack the GluA1 subunit of the AMPA glutamate receptor, encoded by Gria1, a gene recently implicated in schizophrenia by genome-wide association studies. We found that LY354740 failed to rescue the spatial working Memory Deficit in Gria1-/- mice during rewarded alternation performance in the T-maze. In contrast, LY354740 did reduce the locomotor hyperactivity in these animals to a level that was similar to controls. A similar pattern was found with the dopamine receptor antagonist haloperidol, with no amelioration of the spatial working Memory Deficit in Gria1-/- mice, even though the same dose of haloperidol reduced their locomotor hyperactivity. These results with LY354740 contrast with the rescue of spatial working Memory in models of glutamatergic hypofunction using non-competitive NMDAR antagonists. Future studies should determine whether group II mGluR agonists can rescue spatial working Memory Deficits with other NMDAR manipulations, including genetic models and other pharmacological manipulations of NMDAR function.
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Dataset for: The group II metabotropic glutamate receptor agonist LY354740 and the D2 receptor antagonist haloperidol reduce locomotor hyperactivity but fail to rescue spatial working Memory in GluA1 knockout mice
2017Co-Authors: Thomas Boerner, Rolf Sprengel, Peter H. Seeburg, Paul J Harrison, Alexei M. Bygrave, Jingkai Chen, Anushka Fernando, Stephanie Jackson, Chris Barkus, Gary GilmourAbstract:Group II metabotropic glutamate receptor agonists have been suggested as potential anti-psychotics, at least in part, based on the observation that the agonist LY354740 appeared to rescue the cognitive Deficits caused by non-competitive N-methyl-D-aspartate receptor (NMDAR) antagonists, including spatial working Memory Deficits in rodents. Here, we tested the ability of LY354740 to rescue spatial working Memory performance in mice that lack the GluA1 subunit of the AMPA glutamate receptor, encoded by Gria1, a gene recently implicated in schizophrenia by genome-wide association studies. We found that LY354740 failed to rescue the spatial working Memory Deficit in Gria1-/- mice during rewarded alternation performance in the T-maze. In contrast, LY354740 did reduce the locomotor hyperactivity in these animals to a level that was similar to controls. A similar pattern was found with the dopamine receptor antagonist haloperidol, with no amelioration of the spatial working Memory Deficit in Gria1-/- mice, even though the same dose of haloperidol reduced their locomotor hyperactivity. These results with LY354740 contrast with the rescue of spatial working Memory in models of glutamatergic hypofunction using non-competitive NMDAR antagonists. Future studies should determine whether group II mGluR agonists can rescue spatial working Memory Deficits with other NMDAR manipulations, including genetic models and other pharmacological manipulations of NMDAR function
Adrian Ivanoiu - One of the best experts on this subject based on the ideXlab platform.
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increased sensitivity to proactive interference in amnestic mild cognitive impairment is independent of associative and semantic impairment
Brain and Cognition, 2010Co-Authors: Bernard Hanseeuw, Xavier Seron, Adrian IvanoiuAbstract:Episodic Memory Deficit is the hallmark of amnestic mild cognitive impairment (aMCl). There is, however, an overlap in performance among patients with aMCl and elderly controls (EC). The Memory Deficit in aMCl therefore needs to be better characterized. Studies have shown that associative Memory is selectively impaired in aMCl, and recent work suggested that aMCl may be hypersensitive to semantic proactive interference (PI). It is not known whether this increased PI is related to associative or semantic impairment. EC (n = 44) and patients with aMCI (n = 30) performed two tasks presenting a gradually increasing PI effect across four lists. One task used semantic cueing, the other phonological cueing. We controlled for associative Memory by introducing it as a covariate and by matching our subjects for it. Patients with aMCI had a greater PI effect than EC matched for associative Memory, regardless of the type of cueing. The increased PI effect in patients with aMCl is independent of their associative and semantic impairment. (C) 2009 Elsevier Inc. All rights reserved.
Ilhoon Jung - One of the best experts on this subject based on the ideXlab platform.
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ginsenosides rg5 and rh3 protect scopolamine induced Memory Deficits in mice
Journal of Ethnopharmacology, 2013Co-Authors: Eunjin Kim, Ilhoon Jung, Thi Kim Van Le, Jinju Jeong, Namjae Kim, Donghyun KimAbstract:Abstract Ethnopharmacological relevance Panax ginseng (family Araliaceae) is traditionally used as a remedy for cancer, inflammation, stress and aging. Aim of study To explore whether ginsenosides Rg5 and Rh3, the main constituents of heat-processed ginseng (the root of Panax ginseng ), could protect Memory Deficit. Materials and methods We isolated ginsenosides Rh3 and Rg5 from heated-processed ginseng treated with and without human feces, respectively. Then we investigated their protective effects on Memory impairment using the passive avoidance, Y-maze and Morris water maze tasks in mice. Memory Deficit was induced in mice by the intraperitoneal injection of scopolamine. Results Ginsenosides Rg5 or Rh3 increased the latency time reduced by scopolamine in passive avoidance test. Treatment with ginsenoside Rg5 or Rh3 significantly reversed the lowered spontaneous alteration induced by scopolamine in Y-maze task. Ginsenoisde Rg5 or Rh3 (10 mg/kg) significantly shortened the escape latencies prolonged by treatment with scopolamine on the last day of training trial sessions in Morris water maze task. Furthermore, ginsenosides Rg5 and Rh3 inhibited acetylcholinesterase activity in a dose-dependent manner, with IC 50 values of 18.4 and 10.2 μM, respectively. The inhibitory potency of ginsenoside Rh3 is comparable with that of donepezil (IC 50 =9.9 μM). These ginsenosides also reversed hippocampal brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation reduced by scopolamine. Of them, ginsenoside Rh3 more potently protected Memory Deficit. Conclusions Ginsenoside Rg5 and its metabolite ginsenoside Rh3 may protect Memory Deficit by inhibiting AChE activity and increasing BDNF expression and CREB activation.
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lactobacillus pentosus var plantarum c29 protects scopolamine induced Memory Deficit in mice
Journal of Applied Microbiology, 2012Co-Authors: Ilhoon Jung, M A Jung, Eui Jong Kim, Myung Joo Han, Donghyun KimAbstract:Aims In the preliminary study, kimchi, a traditional food fermented with Chinese cabbage, protected scopolamine-induced mouse Memory Deficit in passive avoidance test. Therefore, we screened protective ingredients, particularly lactic acid bacteria, from Chinese cabbage kimchi against scopolamine-induced Memory Deficit in mice. Methods and Results Lactic acid bacteria, isolated from Chinese cabbage kimchi, were identified by 16S rDNA sequence analysis, G+C content and cellular fatty acid composition and sugar fermentation test. Memory Deficit was induced in mice by intraperitoneally injecting with scopolamine. Kimchi, particularly its supernatant, protected scopolamine-induced Memory Deficit in mice in passive avoidance test. Of kimchi ingredients, a lactic acid bacterium, strain C29, potently protected scopolamine-induced Memory Deficit in mice. C29 was a gram-positive, catalase-negative, anaerobic and non-motile rod. Its pylogenetic property was near to Lactobacillus pentosus (99%) and Lact. plantarum (99%). However, C29 fermented inulin and L-rhamnose and grew in pH 3 and at 45°C in contrast with Lact. pentosus and Lact. plantarum. Therefore, it named to be Lact pentosus var. plantarum C29. The strain C29 protected scopolamine-induced Memory Deficit in Y-maze and Morris water maze tests. Furthermore, C29 increased hippocampal BDNF and p-CREB expressions, which were reduced by scopolamine. Conclusion Lactobacillus pentosus var. plantarum C29 may protect Memory Deficit by inducing BDNF and p-CREB expressions. Significance and Impact of the Study Lactic acid bacteria, such as Lact pentosus var. plantarum C29, may prevent Memory Deficit and its contained fermented foods may be beneficial for dementia.