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Author (up) Burgos-Ramos, E.; Chowen, J.A.; Argente, J.; Barrios, V. file  url
openurl 
  Title Regional and temporal differences in leptin signaling in rat brain Type Journal Article
  Year 2010 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol  
  Volume 167 Issue 1 Pages 143-152  
  Keywords Animals; Blotting, Western; Brain/*metabolism; Cerebellum/metabolism; Hippocampus/metabolism; Hypothalamus/metabolism; Leptin/*metabolism; Male; Radioimmunoprecipitation Assay; Rats; Rats, Wistar; Signal Transduction/*physiology; Time Factors  
  Abstract Leptin regulates energy homeostasis through activation of different hypothalamic pathways. Evidence indicates that leptin is a pleiotropic hormone that acts on many brain areas, altering food intake, metabolism, and locomotion, among other functions. Because short-term effects of leptin infusion and intracellular pathways in other brain areas involved in food regulation have not been thoroughly analysed, we have studied the acute effect of intracerebroventricular leptin administration on the levels of the long form of leptin receptor (Ob-Rb), as well as on activation of Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3), protein kinase B (Akt), extracellular regulated kinases (ERKs) and levels of suppressor of cytokine signaling-3 (SOCS3) in the hypothalamus, hippocampus, frontal cortex and cerebellum of adult male Wistar rats at 15min, 1 and 6h. The levels of Ob-Rb increased at 6h in hypothalamus only. Leptin activated the JAK2/STAT3 pathway in all areas, although in a temporally specific pattern. In contrast, this hormone decreased Akt activation in hypothalamus, hippocampus and cerebellum and ERK activation in frontal cortex, while it increased ERK activation in hypothalamus and hippocampus. These differences in modulation of Ob-Rb levels and signaling indicate that the rapid effects of leptin in non-hypothalamic areas are mediated, at least in part, through the intracellular pathways involved in hypothalamic energy balance, but in a temporally specific manner.  
  Call Number Serial 218  
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Author (up) Chen, X.; D'Souza, R.; Hong, S.-T. file  url
openurl 
  Title The role of gut microbiota in the gut-brain axis: current challenges and perspectives Type Journal Article
  Year 2013 Publication Protein & Cell Abbreviated Journal Protein Cell  
  Volume 4 Issue 6 Pages 403-414  
  Keywords Brain/*metabolism; Central Nervous System/metabolism; Gastrointestinal Tract/*metabolism/microbiology; High-Throughput Nucleotide Sequencing; Humans; Liver/metabolism; Metabolic Diseases/metabolism/pathology; *Metagenome; Microbiome; Receptors, G-Protein-Coupled/metabolism  
  Abstract Brain and the gastrointestinal (GI) tract are intimately connected to form a bidirectional neurohumoral communication system. The communication between gut and brain, knows as the gut-brain axis, is so well established that the functional status of gut is always related to the condition of brain. The researches on the gut-brain axis were traditionally focused on the psychological status affecting the function of the GI tract. However, recent evidences showed that gut microbiota communicates with the brain via the gut-brain axis to modulate brain development and behavioral phenotypes. These recent findings on the new role of gut microbiota in the gut-brain axis implicate that gut microbiota could associate with brain functions as well as neurological diseases via the gut-brain axis. To elucidate the role of gut microbiota in the gut-brain axis, precise identification of the composition of microbes constituting gut microbiota is an essential step. However, identification of microbes constituting gut microbiota has been the main technological challenge currently due to massive amount of intestinal microbes and the difficulties in culture of gut microbes. Current methods for identification of microbes constituting gut microbiota are dependent on omics analysis methods by using advanced high tech equipment. Here, we review the association of gut microbiota with the gut-brain axis, including the pros and cons of the current high throughput methods for identification of microbes constituting gut microbiota to elucidate the role of gut microbiota in the gut-brain axis.  
  Call Number Serial 2005  
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Author (up) Mori, N.; Mori, M. file  url
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  Title Neuronal Shc: a gene of longevity in the brain? Type Journal Article
  Year 2011 Publication Medical Hypotheses Abbreviated Journal Med Hypotheses  
  Volume 77 Issue 6 Pages 996-999  
  Keywords Animals; *Biological Evolution; Brain/*metabolism; Brain-Derived Neurotrophic Factor/metabolism; Humans; *Longevity; Mammals/genetics/*physiology; N-Methylaspartate/metabolism; Neurons/*metabolism; Quality of Life; Shc Signaling Adaptor Proteins/*metabolism  
  Abstract Aging is inevitable to all multi-cellular organisms, and each organism has its own lifespan. The species-specific lifespan seems determined genetically; however little is known about how the lifespan determined. During the last decades accumulative evidence indicates that there is certainly a set of genes that are involved in the lifespan determination. Among those dozens of genes, the Shc gene encoding a phosphotyrosine signal adaptor is of potential interests in mammalian aging and/or longevity determination. Shc is merely one form of a gene family, and accumulative evidence demonstrates the presence of additional Shc homologues that are strongly expressed in the nervous system. We hypothesize that lifespan is regulated primarily by the nervous system and/or brain, and neurally expressed Shc homologues play pivotal roles in relation to the evolution of longevity with quality of life. We discuss herein the recent progress of our understanding of the neuronally expressed Shc genes in comparision with p66-Shc as a candidate for the evolution of long life with higher quality of life in mammals.  
  Call Number Serial 109  
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Author (up) Nagatsu, T. file  url
openurl 
  Title Isoquinoline neurotoxins in the brain and Parkinson's disease Type Journal Article
  Year 1997 Publication Neuroscience Research Abbreviated Journal Neurosci Res  
  Volume 29 Issue 2 Pages 99-111  
  Keywords Brain/*metabolism; Humans; Isoquinolines/chemistry/*metabolism; Neurotoxins/*metabolism; Parkinson Disease/*metabolism; Tyrosine 3-Monooxygenase/antagonists & inhibitors  
  Abstract Parkinson's disease is thought to be caused by some unknown endogenous or exogenous factors interacting with genetic dispositions. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an exogenous neurotoxin producing parkinsonism in humans, monkeys and various animals as the result of monoamine oxidase type B (MAO-B)-catalyzed conversion of it to the 1-methyl-4-phenyl-pyridinium ion (MPP+), which selectively kills the nigrostriatal dopaminergic neurons. Various isoquinoline derivatives were found in the brain of patients with Parkinson's disease. Isoquinoline derivatives have neurochemical properties similar to those of MPTP and they are considered to be the endogenous neurotoxins which cause Parkinson's disease. Among them, tetrahydroisoquinoline (TIQ), 1-benzyl-TIQ, and (R)-1,2-dimethyl-5,6-dihydroxy-TIQ [(R)-N-methyl-salsolinol)] have the most potent neurotoxicity. TIQs, like MPTP, may be activated via N-methylation by N-methyltransferase and oxidation by MAO. TIQs as well as MPP+ inhibit complex I of the electron transport system in mitochondria, thereby reducing ATP formation and producing oxygen radicals. Although the properties of TIQs are similar to those of MPTP, the neurotoxicity of TIQs is weaker than that of MPTP. Since Parkinson's disease is a slowly progressing neurodegenerative disease, long term neurotoxic effects of IQs remain to be further examined in primates.  
  Call Number Serial 87  
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