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Clavulanic acid protects neurons in pharmacological models of neurodegenerative diseases
Huh, Youngbuhm,Ju, Mi Sun,Park, Hanbyeol,Han, Shengjun,Bang, Yu-Mi,Ferris, Craig F.,Koppell, Gary A.,King, Jean A.,Kim, Minkyu Leo,Kim, Deog Joong,Ahn, Chang Ho,Oh, Myung-Sook Wiley Subscription Services, Inc., A Wiley Company 2010 Drug development research Vol.71 No.6
<P>Clavulanic acid is a psychoactive compound with excellent blood-brain barrier permeability and safety profiles. Previous studies showed that clavulanic acid suppresses anxiety in rodents and in a primate model. In addition, clavulanic acid is thought to enhance sexual function in animal models via central nervous system (CNS) mechanisms. To further examine its potential as a CNS-modulating agent, we investigated the effects of clavulanic acid in neurotoxin-induced animal models that emulate neurodegenerative disease symptoms. Clavulanic acid was administered to rodents that were exposed to kainic acid or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Using histochemical staining of brain sections, we demonstrated that clavulanic acid protects hippocampal and dopaminergic neurons from toxin-induced acute death. We also observed that clavulanic acid improves motor function in MPTP-treated mice in a behavioral test. These data indicate that clavulanic acid may have neuroprotective effects and warrants further investigation of its therapeutic use in CNS disorders, such as Parkinson's and Alzheimer's disease. Drug Dev Res 71:351–357, 2010. © 2010 Wiley-Liss, Inc.</P>
Gene transfer in the nervous system and implications for transsynaptic neuronal tracing.
Huh, Youngbuhm,Oh, Myung S,Leblanc, Pierre,Kim, Kwang-Soo Ashley Publications Ltd 2010 Expert opinion on biological therapy Vol.10 No.5
<P>IMPORTANCE OF THE FIELD: Neuronal circuitries are determined by specific synaptic connections and they provide the cellular basis of cognitive processes and behavioral functions. To investigate neuronal circuitries, tracers are typically used to identify the original neurons and their projection targets. AREAS COVERED IN THIS REVIEW: Traditional tracing methods using chemical tracers have major limitations such as non-specificity. In this review, we highlight novel genetic tracing approaches that enable visualization of specific neuronal pathways by introducing cDNA encoding a transsynaptic tracer. In contrast to conventional tracing methods, these genetic approaches use cell-type-specific promoters to express transsynaptic tracers such as wheat germ agglutinin and C-terminal fragment of tetanus toxin, which allows labeling of either the input or output populations and connections of specific neuronal type. WHAT THE READER WILL GAIN: Specific neuronal circuit information by these genetic approaches will allow more precise, comprehensive and novel information about individual neural circuits and their function in normal and diseased brains. TAKE HOME MESSAGE: Using tracer gene transfer, neuronal circuit plasticity after traumatic injury or neurodegenerative diseases can be visualized. Also, this can provide a good marker for evaluation of therapeutic effects of neuroprotective or neurotrophic agents.</P>
Moon, Minho,Huh, Youngbuhm,Park, Chan Lippincott Williams Wilkins, Inc. 2006 NEUROREPORT - Vol.17 No.11
Voluntary exercise such as running induces a dramatic increase in adult stem cell proliferation within the dentate gyrus, and endothelial nitric oxide synthase helps regulate cell proliferation. The role of endothelial nitric oxide synthase in exercise-induced cell proliferation in the brain, however, has not been examined. In the present study, exercise for 1 week increased endothelial nitric oxide synthase and nicotinamide adenine dinucleotide phosphate-diaphorase immunoreactivity in the microvessels of the dentate gyrus. In addition, blocking endothelial nitric oxide synthase activity (via a daily injection of 20 mg/kg L-nitroimidazole ornithine) during exercise reduced the number of cells within the dentate gyrus that were immunoreactive for Ki-67 protein and doublecortin. This study provides the first evidence that endothelial nitric oxide synthase upregulation may modulate exercise-induced granule cell proliferation within the dentate gyrus.
The Expressional Changes of Nitric Oxide Synthase in the Rat Brain Following Food Restriction
Kang Kyounglan,Huh Youngbuhm,Park Chan,Choue Ryo Won The Korean Nutrition Society 2005 Nutritional Sciences Vol.8 No.4
This study investigated the changes in the neuronal nitric oxide synthase (nNOS) and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) activities during food restriction in the rat brain such as cerebral cortex, cerebellum, caudate pautamen and hypothalamus. The rats were placed on a restricted feeding schedule consisting of half the ad libitum quantity for 3 days and 1, 2, 4, 6 and 9 weeks, and a free feeding schedule for 4 weeks. The loss of body weight peaked after 1 week of food restriction and persisted during the entire 9-week period of food restriction. The dramatic weight change in the first week ($12\%$) and the reduction in weight changes thereafter suggest that major adaptation changes occur early and body maintenance occurs subsequently. In the hypothalamus, the optical densities of the NADPH-d and nNOS immunoreactivities were found to be significantly higher in the 1-week and lower in the 9-week food restricted group than in the ad libitum fed control rats. In contrast, in the cerebral cortex, the optical densities of the NADPH-d- and nNOS-positive neurons were not changed significantly during the period of food restriction. This study provides the morphological evidence showing that food restriction has a significant effect on the nitric oxide synthesizing system of the hypothalamus.
Kim Na Hee,Huh Youngbuhm,Kim Dokyoung 대한화학회 2022 Bulletin of the Korean Chemical Society Vol.43 No.6
Here, we disclose a new turn-on type fluorescent probe (named BCB-1) for the detection of Aβ plaques, which is an essential biomarker in Alzheimer’s disease (AD). BCB-1 has a hybrid structure of benzo[g]coumarin and benzothiazole, and it showed significant emission enhancement at the near-infrared (NIR) region when sensing Aβ plaques. BCB-1 also showed high selectivity and sensitivity toward Aβ plaques, and its bio-imaging applicability was confirmed within an AD mouse (5XFAD) brain. We expect our superb AD diagnosis fluorescent probe to be broadly applied in Aβ plaques related clinical and biological studies.