Inhibition, but Not Excitation, Recovers From Partial Cone Loss With Greater Spatiotemporal Integration, Synapse Density and Frequency

2021 ◽  
Author(s):  
Joo Yeun Lee ◽  
Rachel A. Care ◽  
David B. Kastner ◽  
Luca Della Santina ◽  
Felice Dunn

Circulation ◽  
1997 ◽  
Vol 95 (4) ◽  
pp. 932-939 ◽  
Author(s):  
Jing Ping Sun ◽  
Min Pu ◽  
Fetnat M. Fouad ◽  
Raymond Christian ◽  
William J. Stewart ◽  
...  


Author(s):  
Fei Wang ◽  
Qianqian Wang ◽  
Baowei Liu ◽  
Lisheng Mei ◽  
Sisi Ma ◽  
...  

AbstractThe brain is known to express many long noncoding RNAs (lncRNAs); however, whether and how these lncRNAs function in modulating synaptic stability remains unclear. Here, we report a cerebellum highly expressed lncRNA, Synage, regulating synaptic stability via at least two mechanisms. One is through the function of Synage as a sponge for the microRNA miR-325-3p, to regulate expression of the known cerebellar synapse organizer Cbln1. The other function is to serve as a scaffold for organizing the assembly of the LRP1-HSP90AA1-PSD-95 complex in PF-PC synapses. Although somewhat divergent in its mature mRNA sequence, the locus encoding Synage is positioned adjacent to the Cbln1 loci in mouse, rhesus macaque, and human, and Synage is highly expressed in the cerebella of all three species. Synage deletion causes a full-spectrum cerebellar ablation phenotype that proceeds from cerebellar atrophy, through neuron loss, on to synapse density reduction, synaptic vesicle loss, and finally to a reduction in synaptic activity during cerebellar development; these deficits are accompanied by motor dysfunction in adult mice, which can be rescued by AAV-mediated Synage overexpression from birth. Thus, our study demonstrates roles for the lncRNA Synage in regulating synaptic stability and function during cerebellar development.





2006 ◽  
Vol 174 (2) ◽  
pp. 289-299 ◽  
Author(s):  
Shernaz X. Bamji ◽  
Beatriz Rico ◽  
Nikole Kimes ◽  
Louis F. Reichardt

Neurons of the vertebrate central nervous system have the capacity to modify synapse number, morphology, and efficacy in response to activity. Some of these functions can be attributed to activity-induced synthesis and secretion of the neurotrophin brain-derived neurotrophic factor (BDNF); however, the molecular mechanisms by which BDNF mediates these events are still not well understood. Using time-lapse confocal analysis, we show that BDNF mobilizes synaptic vesicles at existing synapses, resulting in small clusters of synaptic vesicles “splitting” away from synaptic sites. We demonstrate that BDNF's ability to mobilize synaptic vesicle clusters depends on the dissociation of cadherin–β-catenin adhesion complexes that occurs after tyrosine phosphorylation of β-catenin. Artificially maintaining cadherin–β-catenin complexes in the presence of BDNF abolishes the BDNF-mediated enhancement of synaptic vesicle mobility, as well as the longer-term BDNF-mediated increase in synapse number. Together, this data demonstrates that the disruption of cadherin–β-catenin complexes is an important molecular event through which BDNF increases synapse density in cultured hippocampal neurons.



1993 ◽  
Vol 49 (8) ◽  
pp. 1537-1540 ◽  
Author(s):  
G. Ferguson ◽  
J. F. Gallagher ◽  
S. Pappalardo
Keyword(s):  


1993 ◽  
Vol 53 (2) ◽  
pp. 190-199 ◽  
Author(s):  
Romy V. Spitz ◽  
Joan Stiles ◽  
Ralph M. Siegel


2008 ◽  
Vol 45 (25-26) ◽  
pp. 6301-6315 ◽  
Author(s):  
George Levesque ◽  
Nagaraj K. Arakere
Keyword(s):  


2000 ◽  
Vol 65 (24) ◽  
pp. 8283-8289 ◽  
Author(s):  
Jean Guillon ◽  
Jean-Michel Léger ◽  
Pascal Sonnet ◽  
Christian Jarry ◽  
Max Robba
Keyword(s):  


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