Mice deficient in nervous system-specific carbohydrate epitope HNK-1 exhibit impaired synaptic plasticity and spatial learning.
Shoji Yamamoto,Shogo Oka,Mitsuhiro Inoue,Misa Shimuta,Toshiya Manabe,Hideki Takahashi,Masaomi Miyamoto,Masahide Asano,Junko Sakagami,Katsuko Sudo,Yoichiro Iwakura,Katsuhiko Ono,Toshisuke Kawasaki +12 more
TLDR
It is shown that the loss of a single non-reducing terminal carbohydrate residue attenuates brain higher functions in mice generated with a targeted deletion of the GlcAT-P gene.About:
This article is published in Journal of Biological Chemistry.The article was published on 2002-07-26 and is currently open access. It has received 138 citations till now. The article focuses on the topics: Long-term potentiation & Synaptic plasticity.read more
Citations
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Glycans and neural cell interactions
Ralf Kleene,Melitta Schachner +1 more
TL;DR: Carbohydrate-carrying molecules in the nervous system have important roles during development, regeneration and synaptic plasticity and the tremendous structural diversity of glycan chains allows for immense combinatorial possibilities that might underlie the fine-tuning of cell–cell and cell–matrix interactions.
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Extracellular matrix molecules and synaptic plasticity
TL;DR: It is hypothesized that ECM molecules derived from neurons and glia might also shape synaptic plasticity through regulation of organelle trafficking, and by imposing diffusion constraints for neurotransmitters and trophic factors.
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Widespread Disruption of Repressor Element-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor Occupancy at Its Target Genes in Huntington's Disease
Chiara Zuccato,Nikolai D. Belyaev,Paola Conforti,Lezanne Ooi,Marzia Tartari,Evangelia Papadimou,Marcy E. MacDonald,Elisa Fossale,Scott Zeitlin,Noel J. Buckley,Elena Cattaneo +10 more
TL;DR: The same molecular phenotype is produced in cells and brain tissue depleted of endogenous huntingtin, thereby directly validating the loss-of-function hypothesis of HD, and suggesting that relief of REST/NRSF mediated repression can restore aberrant neuronal gene transcription in HD.
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The role of glycosphingolipid metabolism in the developing brain.
TL;DR: Glycosphingolipids (GSLs) are amphipathic lipids ubiquitously expressed in all vertebrate cells and body fluids, but they are especially abundant in the nervous system.
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Developmental changes of glycosphingolipids and expression of glycogenes in mouse brains
TL;DR: It is concluded that the dramatic changes in GSL pattern and content can serve as useful markers in neural development and that these changes are regulated primarily at the level of glycosyltransferase gene expression.
References
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Developments of a water-maze procedure for studying spatial learning in the rat
TL;DR: Developments of an open-field water-maze procedure in which rats learn to escape from opaque water onto a hidden platform are described, suggesting that they may lend themselves to a variety of behavioural investigations, including pharmacological work and studies of cerebral function.
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Targeted disruption of the c-src proto-oncogene leads to osteopetrosis in mice
TL;DR: It is demonstrated that src is not required for general cell viability (possibly because of functional overlap with other tyrosine kinases related to src) and an essential role for src in bone formation is uncovered.
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Generation and analysis of interleukin-4 deficient mice.
TL;DR: Some but not all of the in vitro properties of IL-4 are critical for the physiology of the immune system in vivo, but the serum levels of IgG1 and IgE are strongly reduced.
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Inactivation of the N-CAM gene in mice results in size reduction of the olfactory bulb and deficits in spatial learning.
Harold Cremer,Rita Lange,Annette Christoph,Markus Plomann,Gaby Vopper,Jürgen Roes,Russell W. Brown,Stanley A. Baldwin,Philipp J. Kraemer,Stephen W. Scheff +9 more
TL;DR: It is shown here that N-CAM-deficient mice generated by gene targeting appear healthy and fertile, but adult mutants show a 10% reduction in overall brain weight and a 36% decline in size of the olfactory bulb.
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Negative regulation of T-cell activation and autoimmunity by Mgat5 N -glycosylation
TL;DR: It is demonstrated that a deficiency in β1,6 N-acetylglucosaminyltransferase V (Mgat5), an enzyme in the N-glycosylation pathway, lowers T-cell activation thresholds by directly enhancing TCR clustering.