Neuroligin-induced presynaptic differentiation through SLM2-mediated splicing modifications of neurexin in cerebellar cultures

2017 ◽  
Vol 493 (2) ◽  
pp. 1030-1036 ◽  
Author(s):  
Yuji Sato ◽  
Satoko Suzuki ◽  
Yoko Iijima ◽  
Takatoshi Iijima
Keyword(s):  
Presynaptic Differentiation ◽  
Cerebellar Cultures

scholarly journals In Vivo Imaging of Dorsal Root Regeneration: Rapid Immobilization and Presynaptic Differentiation at the CNS/PNS Border

2011 ◽  
Vol 31 (12) ◽  
pp. 4569-4582 ◽  
Author(s):  
A. Di Maio ◽  
A. Skuba ◽  
B. T. Himes ◽  
S. L. Bhagat ◽  
J. K. Hyun ◽  
...  
Keyword(s):  
In Vivo Imaging ◽  
Dorsal Root ◽  
Root Regeneration ◽  
Presynaptic Differentiation

scholarly journals Local protein synthesis of neuronal MT1-MMP for agrin-induced presynaptic development

Development ◽  
2021 ◽  
Vol 148 (10) ◽  
Author(s):  
Jun Yu ◽  
Marilyn Janice Oentaryo ◽  
Chi Wai Lee
Keyword(s):  
Protein Synthesis ◽  
Neuronal Development ◽  
Neuromuscular Junctions ◽  
Neuronal Cell ◽  
Time Lapse ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Local Protein Synthesis ◽  
Presynaptic Differentiation ◽  
Local Protein

ABSTRACT Upon the stimulation of extracellular cues, a significant number of proteins are synthesized distally along the axon. Although local protein synthesis is crucial for various stages throughout neuronal development, its involvement in presynaptic differentiation at developing neuromuscular junctions remains unknown. By using axon severing and microfluidic chamber assays, we first showed that treatment of a protein synthesis inhibitor, cycloheximide, inhibits agrin-induced presynaptic differentiation in cultured Xenopus spinal neurons. Newly synthesized proteins are prominently detected, as revealed by the staining of click-reactive cell-permeable puromycin analog O-propargyl-puromycin, at agrin bead-neurite contacts involving the mTOR/4E-BP1 pathway. Next, live-cell time-lapse imaging demonstrated the local capturing and immobilization of ribonucleoprotein granules upon agrin bead stimulation. Given that our recent study reported the roles of membrane-type 1 matrix metalloproteinase (MT1-MMP) in agrin-induced presynaptic differentiation, here we further showed that MT1-MMP mRNA is spatially enriched and locally translated at sites induced by agrin beads. Taken together, this study reveals an essential role for axonal MT1-MMP translation, on top of the well-recognized long-range transport of MT1-MMP proteins synthesized from neuronal cell bodies, in mediating agrin-induced presynaptic differentiation.

Loss of GABAergic neuronal phenotype in primary cerebellar cultures following blockade of glutamate reuptake

2003 ◽  
Vol 977 (2) ◽  
pp. 209-220 ◽  
Author(s):  
Attila D. Kovács ◽  
Gvido Cebers ◽  
Aleta Cebere ◽  
Sture Liljequist
Keyword(s):  
Neuronal Phenotype ◽  
Cerebellar Cultures

Enhanced Calcium Transients in Glial Cells in Neonatal Cerebellar Cultures Derived from S100B Null Mice

2000 ◽  
Vol 257 (2) ◽  
pp. 281-289 ◽  
Author(s):  
Zhi-gang Xiong ◽  
David O'Hanlon ◽  
Laurence E. Becker ◽  
John Roder ◽  
John F. MacDonald ◽  
...  
Keyword(s):  
Glial Cells ◽  
Calcium Transients ◽  
Cerebellar Cultures

scholarly journals The proteasome controls presynaptic differentiation through modulation of an on-site pool of polyubiquitinated conjugates

2016 ◽  
Vol 212 (7) ◽  
pp. 789-801 ◽  
Author(s):  
Maria J. Pinto ◽  
Pedro L. Alves ◽  
Luís Martins ◽  
Joana R. Pedro ◽  
Hyun R. Ryu ◽  
...  
Keyword(s):  
Synaptic Vesicles ◽  
Proteasome Inhibition ◽  
Ubiquitin Proteasome System ◽  
Presynaptic Terminal ◽  
Ubiquitinated Proteins ◽  
Presynaptic Differentiation ◽  
Intrinsic Mechanism ◽  
Ubiquitin Proteasome ◽  
Presynaptic Assembly ◽  
Local Modulation

Differentiation of the presynaptic terminal is a complex and rapid event that normally occurs in spatially specific axonal regions distant from the soma; thus, it is believed to be dependent on intra-axonal mechanisms. However, the full nature of the local events governing presynaptic assembly remains unknown. Herein, we investigated the involvement of the ubiquitin–proteasome system (UPS), the major degradative pathway, in the local modulation of presynaptic differentiation. We found that proteasome inhibition has a synaptogenic effect on isolated axons. In addition, formation of a stable cluster of synaptic vesicles onto a postsynaptic partner occurs in parallel to an on-site decrease in proteasome degradation. Accumulation of ubiquitinated proteins at nascent sites is a local trigger for presynaptic clustering. Finally, proteasome-related ubiquitin chains (K11 and K48) function as signals for the assembly of presynaptic terminals. Collectively, we propose a new axon-intrinsic mechanism for presynaptic assembly through local UPS inhibition. Subsequent on-site accumulation of proteins in their polyubiquitinated state triggers formation of presynapses.

scholarly journals The function of p120 catenin in filopodial growth and synaptic vesicle clustering in neurons

2012 ◽  
Vol 23 (14) ◽  
pp. 2680-2691 ◽  
Author(s):  
Cheng Chen ◽  
Pan P. Li ◽  
Raghavan Madhavan ◽  
H. Benjamin Peng
Keyword(s):  
Synaptic Vesicle ◽  
Motor Neurons ◽  
Rho Gtpases ◽  
Acetylcholine Receptors ◽  
Physical Contact ◽  
Spinal Neurons ◽  
P120 Catenin ◽  
Presynaptic Differentiation ◽  
Nerve Muscle ◽  
Postsynaptic Differentiation

At the developing neuromuscular junction (NMJ), physical contact between motor axons and muscle cells initiates presynaptic and postsynaptic differentiation. Using Xenopus nerve–muscle cocultures, we previously showed that innervating axons induced muscle filopodia (myopodia), which facilitated interactions between the synaptic partners and promoted NMJ formation. The myopodia were generated by nerve-released signals through muscle p120 catenin (p120ctn), a protein of the cadherin complex that modulates the activity of Rho GTPases. Because axons also extend filopodia that mediate early nerve–muscle interactions, here we test p120ctn's function in the assembly of these presynaptic processes. Overexpression of wild-type p120ctn in Xenopus spinal neurons leads to an increase in filopodial growth and synaptic vesicle (SV) clustering along axons, whereas the development of these specializations is inhibited following the expression of a p120ctn mutant lacking sequences important for regulating Rho GTPases. The p120ctn mutant also inhibits the induction of axonal filopodia and SV clusters by basic fibroblast growth factor, a muscle-derived molecule that triggers presynaptic differentiation. Of importance, introduction of the p120ctn mutant into neurons hinders NMJ formation, which is observed as a reduction in the accumulation of acetylcholine receptors at innervation sites in muscle. Our results suggest that p120ctn signaling in motor neurons promotes nerve–muscle interaction and NMJ assembly.

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