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Neuronal Surface (neuronal + surface)
Selected AbstractsRegulation of NMDA receptor trafficking and function by striatal-enriched tyrosine phosphatase (STEP)EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2006Steven P. Braithwaite Abstract Regulation of N -methyl- d -aspartate (NMDA) receptors is critical for the normal functioning of the central nervous system. There must be precise mechanisms to allow for changes in receptor function required for learning and normal synaptic transmission, but within tight constraints to prevent pathology. Tyrosine phosphorylation is a major means by which NMDA receptors are regulated through the equilibrium between activity of Src family kinases and tyrosine phosphatases. Identification of NMDA receptor phosphatases has been difficult, the best candidate being striatal-enriched tyrosine phosphatase (STEP). Here we demonstrate that STEP is a critical regulator of NMDA receptors and reveal that the action of this tyrosine phosphatase controls the constitutive trafficking of NMDA receptors and leads to changes in NMDA receptor activity at the neuronal surface. We show that STEP binds directly to NMDA receptors in the absence of other synaptic proteins. The activity of STEP selectively affects the expression of NMDA receptors at the neuronal plasma membrane. The result of STEP's action upon the NMDA receptor affects the functional properties of the receptor and its downstream signaling. These effects are evident when STEP levels are chronically reduced, indicating that there is no redundancy amongst phosphatases to compensate for altered STEP function in the CNS. STEP may have evolved specifically to fill a pivotal role as the NMDA receptor phosphatase, having a distinct and restricted localization and compartmentalization, and unique activity towards the NMDA receptor and its signaling pathway. [source] Transgenic mice expressing a dual, CRE-inducible reporter for the analysis of axon guidance and synaptogenesis,GENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 6 2007Aurora Badaloni Abstract Improved and modular tools are needed for the neuroanatomical dissection of CNS axonal tracts, and to study the cell-intrinsic and cell-extrinsic cues that govern their assembly and plasticity. Here we describe a general purpose transgenic tracer that can be used to visualize axonal tracts and synaptic terminals in any region of the embryonic neural tube or postnatal CNS, on any wild type or mutant genetic background. The construct permits CRE-inducible expression of a dicistronic axonal marker encoding two surface reporter proteins: a farnesylated GFP and the human Placental Alkaline Phosphatase (PLAP). Both proteins localize alongside the neuronal surface, permitting the concomitant detection of cell body, neurites, and presynaptic and postsynaptic sites in the same neuron. This provides a CRE-inducible dual system for imaging neural circuits in vivo, and to study their assembly and remodeling in cultured neurons, neural stem cells, and tissue explants derived from the reporter line. Unlike existing lines, this reporter does not encode a ubiquitously expressed, floxable LacZ gene, permitting the simultaneous analysis of beta galactosidase activity in mutant lines. genesis 45:405,412, 2007. © 2007 Wiley-Liss, Inc. [source] Immunization with a cannabinoid receptor type 1 peptide results in experimental allergic meningocerebellitis in the Lewis rat: A model for cell-mediated autoimmune neuropathology,JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2002Margit G. Proescholdt Abstract Neuronal elements are increasingly suggested as primary targets of an autoimmune attack in certain neurological and neuropsychiatric diseases. Type 1 cannabinoid receptors (CB1) were selected as autoimmune targets because they are predominantly expressed on neuronal surfaces in brain and display strikingly high protein levels in striatum, hippocampus, and cerebellum. Female Lewis rats were immunized with N-terminally acetylated peptides (50 or 400 ,g per rat) of the extracellular domains of the rat CB1 and killed at various time points. Subsequent evaluation using immunohistochemistry and in situ hybridization showed dense infiltration of immune cells exclusively within the cerebellum, peaking 12,16 days after immunization with the CB1 peptide containing amino acids 9,25. The infiltrates clustered in meninges and perivascular locations in molecular and granular cell layers and were also scattered throughout the CB1-rich neuropil. They consisted primarily of CD4+ and ED1+ cells, suggestive of cell-mediated autoimmune pathology. There were no inflammatory infiltrates elsewhere in the brain or spinal cord. The results show that neuronal elements, such as neuronal cell-surface receptors, may be recognized as antigenic targets in a cell-mediated autoimmune attack and, therefore, support the hypothesis of cell-mediated antineuronal autoimmune pathology in certain brain disorders. Published 2002 Wiley-Liss, Inc. [source] Fine structure of neuronal and glial processes in neuropathologyNEUROPATHOLOGY, Issue 1 2006Asao Hirano The cells of the nervous system are characterized by their well-formed cell processes and by cell-to-cell relationships that they form. The neuron reveals essentially cylindrical processes, which form synaptic junctions. On the other hand, the peripheral parts of the glial cells are mainly sheet-like in nature. Thus, the oligodendroglial cell elaborates many sheet-like processes, each of which forms a segment of the myelin sheath. Unique cell junction, transverse bands are present at the interface of oligodendroglial processes and the axon. Finally, the astrocytes also form elaborate sheet-like processes, which separate most of the CNS from the mesodermal tissue as well as surrounding certain neuronal surfaces, including synapses. Punctate adhesions, gap junctions and other adhesive devices are present between astrocytic processes. Defects or anomalies in the neuronal and glial cell processes characterize numerous pathological conditions. [source] | ||||||||||