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Author (up) Baylis, H.A.; Furuichi, T.; Yoshikawa, F.; Mikoshiba, K.; Sattelle, D.B. file  url
openurl 
  Title Inositol 1,4,5-trisphosphate receptors are strongly expressed in the nervous system, pharynx, intestine, gonad and excretory cell of Caenorhabditis elegans and are encoded by a single gene (itr-1) Type Journal Article
  Year 1999 Publication Journal of Molecular Biology Abbreviated Journal J Mol Biol  
  Volume 294 Issue 2 Pages 467-476  
  Keywords Amino Acid Sequence; Animals; Animals, Genetically Modified; Binding Sites; Caenorhabditis elegans/*genetics; Calcium Channels/*genetics/*metabolism; Cell Membrane/genetics/metabolism; Conserved Sequence; Gene Expression Profiling; Gonads/metabolism; Helminth Proteins/*genetics/*metabolism; Inositol 1,4,5-Trisphosphate Receptors; Intestines/metabolism; Molecular Sequence Data; Nervous System/metabolism; Pharynx/metabolism; RNA, Messenger; Receptors, Cytoplasmic and Nuclear/*genetics/*metabolism; Rectum/cytology/metabolism  
  Abstract Inositol 1,4,5-trisphosphate (InsP3) activates receptors (InsP3Rs) that mediate intracellular Ca(2+ )release, thereby modulating intracellular calcium signals and regulating important aspects of cellular physiology and gene expression. To further our understanding of InsP3Rs we have characterised InsP3Rs and the InsP3R gene, itr-1, from the model organism Caenorhabditis elegans. cDNAs encoding InsP3Rs were cloned enabling us to: (a) identify three putative transcription start sites that result in alternative mRNA 5' ends: (b) detect alternative splicing at three sites and: (c) determine the full genomic organisation of the itr-1 gene. The InsP3R protein (ITR-1) is approximately 42 % identical with known InsP3Rs and possesses conserved structural features. When the putative InsP3 binding domain was expressed in Escherichia coli, specific binding of InsP3 was detected. Using antibodies against ITR-1 we detected a protein of 220 kDa in C. elegans membranes. These antibodies and itr-1::GFP (green fluorescent protein) reporter constructs were used to determine the expression pattern of itr-1 in C. elegans. Strong expression was observed in the intestine, pharynx, nerve ring, excretory cell and gonad. These results demonstrate the high degree of structural and functional conservation of InsP3Rs from nematodes to mammals and the utility of C. elegans as a system for studies on InsP3R mediated signalling.  
  Call Number Serial 309  
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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) de Groat, W.C.; Yoshimura, N. file  url
openurl 
  Title Changes in afferent activity after spinal cord injury Type Journal Article
  Year 2010 Publication Neurourology and Urodynamics Abbreviated Journal Neurourol Urodyn  
  Volume 29 Issue 1 Pages 63-76  
  Keywords Afferent Pathways/metabolism/*physiopathology; Animals; Central Nervous System/metabolism/*physiopathology; Ganglia, Spinal/metabolism/*physiopathology; Genetic Therapy/methods; Humans; Mechanotransduction, Cellular; Nerve Fibers, Myelinated; Nerve Fibers, Unmyelinated; Nerve Growth Factor/metabolism; Neuroanatomical Tract-Tracing Techniques; Neuronal Plasticity; Patch-Clamp Techniques; Pituitary Adenylate Cyclase-Activating Polypeptide/metabolism; Potassium Channels/metabolism; Recovery of Function; Reflex; Sodium Channels/metabolism; Spinal Cord Injuries/complications/metabolism/*physiopathology/therapy; Urinary Bladder/*innervation; Urinary Bladder, Neurogenic/etiology/metabolism/*physiopathology/therapy; *Urination; gamma-Aminobutyric Acid/metabolism  
  Abstract AIMS: To summarize the changes that occur in the properties of bladder afferent neurons following spinal cord injury. METHODS: Literature review of anatomical, immunohistochemical, and pharmacologic studies of normal and dysfunctional bladder afferent pathways. RESULTS: Studies in animals indicate that the micturition reflex is mediated by a spinobulbospinal pathway passing through coordination centers (periaqueductal gray and pontine micturition center) located in the rostral brain stem. This reflex pathway, which is activated by small myelinated (Adelta) bladder afferent nerves, is in turn modulated by higher centers in the cerebral cortex involved in the voluntary control of micturition. Spinal cord injury at cervical or thoracic levels disrupts voluntary voiding, as well as the normal reflex pathways that coordinate bladder and sphincter function. Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. The recovery of bladder function after spinal cord injury is dependent in part on the plasticity of bladder afferent pathways and the unmasking of reflexes triggered by unmyelinated, capsaicin-sensitive, C-fiber bladder afferent neurons. Plasticity is associated with morphologic, chemical, and electrical changes in bladder afferent neurons and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs. CONCLUSIONS: Spinal cord injury at sites remote from the lumbosacral spinal cord can indirectly influence properties of bladder afferent neurons by altering the function and chemical environment in the bladder or the spinal cord.  
  Call Number Serial 2147  
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Author (up) Farr, S.A.; Banks, W.A.; Morley, J.E. file  url
doi  openurl
  Title Effects of leptin on memory processing Type Journal Article
  Year 2006 Publication Peptides Abbreviated Journal Peptides  
  Volume 27 Issue 6 Pages 1420-1425  
  Keywords Animals; Avoidance Learning; Blood-Brain Barrier; Central Nervous System/metabolism; Hippocampus/metabolism; Leptin/chemistry/*metabolism/pharmacology; Male; Maze Learning; Memory/*drug effects; Memory Disorders/metabolism; Mice  
  Abstract Leptin is a peptide hormone secreted by adipose tissue. Studies have shown that leptin crosses the blood-brain barrier (BBB) by a saturable transport system where it acts within the hypothalamus to regulate food intake and energy expenditure. Leptin also acts in the hippocampus where it facilitates the induction of long-term potentiation and enhances NMDA receptor-mediated transmission. This suggests that leptin plays a role in learning and memory. Obese mice and rats, which have leptin receptor deficiency, have impaired spatial learning. In disease states such as diabetes, humans and animals develop leptin resistance at the BBB. This suggests that low leptin levels in the brain may be involved in cognitive deficits associated with diabetes. In the current study, the effects of leptin on post-training memory processing in CD-1 mice were examined. Mice were trained in T-maze footshock avoidance and step down inhibitory avoidance. Immediately after training, mice received bilateral injections of leptin into the hippocampus. Retention was tested 1 week later in the T-maze and 1 day later in step down inhibitory avoidance. Leptin administration improved retention of T-maze footshock avoidance and step down inhibitory avoidance. Leptin administered 24 h after T-maze training did not improve retention when tested 1 week after training. SAMP8 mice at 12 months of age have elevated amyloid-beta protein and impaired learning and memory. We examined the effect of leptin on memory processing in the hippocampus of 4 and 12 months old SAMP8 mice. Leptin improved retention in both 4 and 12 months old SAMP8 mice; 12 month SAMP8 mice required a lower dose to improve memory compared to 4 months SAMP8 mice. The current results indicate that leptin in the hippocampus is involved in memory processing and suggests that low levels of leptin may be involved in cognitive deficits seen in disease states where leptin transport into the CNS is compromised.  
  Call Number Serial 217  
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Author (up) Pickell, L.; Wu, Q.; Wang, X.-L.; Leclerc, D.; Friedman, H.; Peterson, A.C.; Rozen, R. file  url
doi  openurl
  Title Targeted insertion of two Mthfr promoters in mice reveals temporal- and tissue-specific regulation Type Journal Article
  Year 2011 Publication Mammalian Genome : Official Journal of the International Mammalian Genome Society Abbreviated Journal Mamm Genome  
  Volume 22 Issue 11-12 Pages 635-647  
  Keywords Animals; Blood Vessels/metabolism; Central Nervous System/metabolism; Embryo, Mammalian/*metabolism; Female; Genotype; Homocystinuria/*metabolism; Male; Methylenetetrahydrofolate Reductase (NADPH2)/deficiency/*genetics/*metabolism; Mice; Mice, Inbred C57BL; Mice, Transgenic; Muscle Spasticity/*metabolism; Myocardium/metabolism; Placenta/metabolism; Polymorphism, Single Nucleotide; Pregnancy; *Promoter Regions, Genetic; Psychotic Disorders/metabolism; Testis/metabolism  
  Abstract Methylenetetrahydrofolate reductase (MTHFR), a key enzyme in folate metabolism, synthesizes 5-methyltetrahydrofolate, the main circulatory form of folate which is required for maintaining nontoxic levels of homocysteine and providing one-carbon units for methylation. A common 677C --> T variant in MTHFR confers mild MTHFR deficiency and has been associated with a number of human disorders, including neural tube defects and vascular disease. Two promoters of Mthfr, designated as upstream and downstream promoters, are located upstream of a transcription start site cluster and have previously demonstrated cell-specific activities. In this study we used a unique approach for targeted, single-copy transgene insertion to generate transgenic mice carrying a Mthfr upstream or Mthfr downstream promoter-reporter construct located 5' to the endogenous Hprt (hypoxanthine-guanine phosphoribosyltransferase) locus. The Mthfr downstream promoter demonstrated activity in the neural tube, neural crest cells, dorsal root ganglia, heart, and endothelial cells of blood vessels in 10.5-days post coitum embryos and placentas. Upstream promoter activity was absent at this developmental stage. Postnatally, both promoters demonstrated activity in the brain stem, hippocampus, and thalamus of 1-week-old brain that became stronger in the adult. The Mthfr upstream promoter also showed activity in the cerebellum and cerebral cortex. Both promoters were active in male reproductive tissues, including 1-week-old epididymides, and there was upstream promoter-specific activity in the adult testis. Our investigation of Mthfr regulation in an in vivo mouse model revealed temporal- and tissue-specific regulation that supports important roles for MTHFR in the developing embryo, and in postnatal brain and male reproductive tissues.  
  Call Number Serial 304  
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