scholarly journals N-cadherin: stabilizing synapses

2010 ◽  
Vol 189 (3) ◽  
pp. 397-398 ◽  
Author(s):  
Jyothi Arikkath
Keyword(s):  
Cell Adhesion ◽  
Cell Adhesion Molecule ◽  
Synapse Formation ◽  
Structure And Function ◽  
Cellular Mechanisms ◽  
Central Neurons ◽  
Spine Stabilization ◽  
Spine Structure ◽  
And Function ◽  
Spine Dynamics

Spines are sites of excitatory synapse formation in central neurons. Alterations in spine structure and function are widely believed to actively contribute to the cellular mechanisms of learning and memory. In this issue, Mendez et al. (2010. J. Cell Biol. doi:10.1083/jcb.201003007) demonstrate a pivotal role for the cell adhesion molecule N-cadherin in activity-mediated spine stabilization, offering a new mechanism for how spine dynamics and stability are regulated by activity in central neurons.

scholarly journals Regulation of Neural Cell Adhesion Molecule Polysialylation: Evidence for Nontranscriptional Control and Sensitivity to an Intracellular Pool of Calcium

1998 ◽  
Vol 140 (5) ◽  
pp. 1177-1186 ◽  
Author(s):  
Juan L. Brusés ◽  
Urs Rutishauser
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Calcium Ionophore ◽  
Cytosolic Calcium ◽  
Neural Cell ◽  
Ciliary Ganglion ◽  
Cellular Mechanisms ◽  
Neural Cell Adhesion

The up- and downregulation of polysialic acid–neural cell adhesion molecule (PSA–NCAM) expression on motorneurons during development is associated respectively with target innervation and synaptogenesis, and is regulated at the level of PSA enzymatic biosynthesis involving specific polysialyltransferase activity. The purpose of this study has been to describe the cellular mechanisms by which that regulation might occur. It has been found that developmental regulation of PSA synthesis by ciliary ganglion motorneurons is not reflected in the levels of polysialyltransferase-1 (PST) or sialyltransferase-X (STX) mRNA. On the other hand, PSA synthesis in both the ciliary ganglion and the developing tectum appears to be coupled to the concentration of calcium in intracellular compartments. This study documents a calcium dependence of polysialyltransferase activity in a cell-free assay over the range of 0.1–1 mM, and a rapid sensitivity of new PSA synthesis, as measured in a pulse–chase analysis of tissue explants, to calcium ionophore perturbation of intracellular calcium levels. Moreover, the relevant calcium pool appears to be within a specific intracellular compartment that is sensitive to thapsigargin and does not directly reflect the level of cytosolic calcium. Perturbation of other major second messenger systems, such as cAMP and protein kinase–dependent pathways, did not affect polysialylation in the pulse chase analysis. These results suggest that the shuttling of calcium to different pools within the cell can result in the rapid regulation of PSA synthesis in developing tissues.

Cell Adhesion Systems: Molecular Structure and Function in Embriogenesis and Metastasis

1988 ◽  
pp. 235-244
Author(s):  
Brigitte Boyer ◽  
Gordon C. Tucker ◽  
Annie Delouvée ◽  
Jean-Pierre Ouhayoun ◽  
Jean Paul Thiery
Keyword(s):  
Molecular Structure ◽  
Cell Adhesion ◽  
Structure And Function ◽  
And Function ◽  
Molecular Structure And Function

scholarly journals An Autism-Associated Neuroligin-3 Mutation Affects Developmental Synapse Elimination in the Cerebellum

2021 ◽  
Vol 15 ◽  
Author(s):  
Esther Suk King Lai ◽  
Hisako Nakayama ◽  
Taisuke Miyazaki ◽  
Takanobu Nakazawa ◽  
Katsuhiko Tabuchi ◽  
...  
Keyword(s):  
Cell Adhesion Molecule ◽  
Synapse Formation ◽  
Single Point ◽  
Autism Spectrum ◽  
Mutant Mice ◽  
Single Point Mutation ◽  
Synapse Elimination ◽  
Wild Type ◽  
Post Mortem Brain ◽  
And Function

Neuroligin is a postsynaptic cell-adhesion molecule that is involved in synapse formation and maturation by interacting with presynaptic neurexin. Mutations in neuroligin genes, including the arginine to cystein substitution at the 451st amino acid residue (R451C) of neuroligin-3 (NLGN3), have been identified in patients with autism spectrum disorder (ASD). Functional magnetic resonance imaging and examination of post-mortem brain in ASD patients implicate alteration of cerebellar morphology and Purkinje cell (PC) loss. In the present study, we examined possible association between the R451C mutation in NLGN3 and synaptic development and function in the mouse cerebellum. In NLGN3-R451C mutant mice, the expression of NLGN3 protein in the cerebellum was reduced to about 10% of the level of wild-type mice. Elimination of redundant climbing fiber (CF) to PC synapses was impaired from postnatal day 10–15 (P10–15) in NLGN3-R451C mutant mice, but majority of PCs became mono-innervated as in wild-type mice after P16. In NLGN3-R451C mutant mice, selective strengthening of a single CF relative to the other CFs in each PC was impaired from P16, which persisted into juvenile stage. Furthermore, the inhibition to excitation (I/E) balance of synaptic inputs to PCs was elevated, and calcium transients in the soma induced by strong and weak CF inputs were reduced in NLGN3-R451C mutant mice. These results suggest that a single point mutation in NLGN3 significantly influences the synapse development and refinement in cerebellar circuitry, which might be related to the pathogenesis of ASD.

T203. Methylation and Transcription of BAIAP2 and DLG1, Regulators of Dendritic Spine Structure and Function, in the Postmortem Brain of Schizophrenia Subjects

2018 ◽  
Vol 83 (9) ◽  
pp. S207
Author(s):  
Brandon McKinney ◽  
Jennifer Kuflewski ◽  
Ying Ding ◽  
Shahwar Tariq ◽  
David Lewis ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Structure And Function ◽  
Postmortem Brain ◽  
Spine Structure ◽  
And Function
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