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Derivation of completely cell culture-derived mice from early-passage embryonic stem cells.
TLDR
Fully potent early passage R1 cells and the R1-S3 subclone should be very useful not only for ES cell-based genetic manipulations but also in defining optimal in vitro culture conditions for retaining the initial totipotency of ES cells.
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Chemical induction of mGluR5- and protein synthesis--dependent long-term depression in hippocampal area CA1.
TLDR
It is shown that the same form of synaptic modification can be induced by brief application of the selective mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG), which should be useful for biochemical analysis of mGLUR5- and protein synthesis-dependent synaptic modification.
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Mice Lacking Metabotropic Glutamate Receptor 5 Show Impaired Learning and Reduced CA1 Long-Term Potentiation (LTP) But Normal CA3 LTP
TLDR
Long-term potentiation (LTP) in mGluR5 mutants was significantly reduced in the NMDA receptor (NMDAR)-dependent pathways such as the CA1 region and dentate gyrus of the hippocampus, whereas LTP remained intact in the mossy fiber synapses on the CA3 region, an NMDAR-independent pathway.
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A YAC Mouse Model for Huntington’s Disease with Full-Length Mutant Huntingtin, Cytoplasmic Toxicity, and Selective Striatal Neurodegeneration
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Behavioral Phenotypes of Disc1 Missense Mutations in Mice
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Enhanced LTP in Mice Deficient in the AMPA Receptor GluR2
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Myelin-Associated Glycoprotein Is a Myelin Signal that Modulates the Caliber of Myelinated Axons
TLDR
It is demonstrated that mice with a null mutation of the myelin-associated glycoprotein (MAG) gene have a chronic atrophy of myelinated PNS axons that results in paranodal myelin tomaculi and axonal degeneration, and data support a functional role for MAG in modulating the maturation and viability ofMyelinated axons.
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Calcineurin-Mediated LTD of GABAergic Inhibition Underlies the Increased Excitability of CA1 Neurons Associated with LTP
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CAKβ/Pyk2 Kinase Is a Signaling Link for Induction of Long-Term Potentiation in CA1 Hippocampus
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The Receptor Tyrosine Kinase EphB2 Regulates NMDA-Dependent Synaptic Function
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