Freeze-fracture study of the postsynaptic membrane of the cerebellar mossy fiber synapse in the frog

1980 ◽  
Vol 193 (3) ◽  
pp. 689-700 ◽  
Author(s):  
Gary E. Korte ◽  
Jack Rosenbluth
Keyword(s):  
Mossy Fiber ◽  
Freeze Fracture ◽  
Postsynaptic Membrane ◽  
Fracture Study ◽  
Mossy Fiber Synapse

scholarly journals Remodeling of neuronal membranes as an early response to deafferentation. A freeze-fracture study.

1977 ◽  
Vol 75 (3) ◽  
pp. 837-850 ◽  
Author(s):  
R L Gulley ◽  
R J Wenthold ◽  
G R Neises
Keyword(s):  
Freeze Fracture ◽  
Early Response ◽  
Postsynaptic Membrane ◽  
Normal Numbers ◽  
Neuronal Membranes ◽  
Anteroventral Cochlear Nucleus ◽  
Different Types ◽  
Fracture Study ◽  
Early Effects ◽  
Number Of Particles

The early effects of deafferentation on the postsynaptic membrane beneath the end bulb of Held in the anteroventral cochlear nucleus (AVCN) were studied with the freeze-fracture technique. Three distinct responses were seen on the external membrane leaflet after cochlear ablation. Within 12 h the number of nonaggregate particles increased 147% by the addition of new particles to the membrane. The increase in number of nonaggregate particles continued until 4 days after cochlear ablation. The other responses occurred later, after degenerative changes were present in the end bulb. Between 1 and 2 days after cochlear ablation, the number of perisynaptic aggregates surrounding the postsynaptic active zone decreased to 10% of normal numbers. By 4 days, all perisynaptic aggregates had disappeared from the membrane. Coated vesicles may be involved in removing these aggregates. Between 1 and 3 days, the number of junctional aggregates decreased, but the size of the aggregates increased, apparently as a result of coalescence of nearby junctional aggregates. The total number of particles in junctional aggregates in the membrane was not altered during the first 6 days after cochlear ablation. The three separate responses suggest the existence of at least three different types of intramembranous particles on the external leaflet of the principal cell membrane, with each type dependent upon different cues for its maintenance in the membrane.

Junctional Pattern in the Squamous Metaplasia of the Female Trigone. A Freeze-Fracture Study

1983 ◽  
Vol 129 (2) ◽  
pp. 280-283 ◽  
Author(s):  
M. Sideri ◽  
G. De Virgiliis ◽  
R. Rainoldi ◽  
A. Ferrari ◽  
G. Remotti
Keyword(s):  
Squamous Metaplasia ◽  
Freeze Fracture ◽  
Fracture Study

Freeze-fracture study of the mechanoreceptive digital corpuscles of mice

1985 ◽  
Vol 14 (6) ◽  
pp. 1037-1052 ◽  
Author(s):  
Chizuka Ide ◽  
Kenichi Kumagai ◽  
Schuichiro Hayashi
Keyword(s):  
Freeze Fracture ◽  
Fracture Study

scholarly journals The intellectual disability gene Kirrel3 regulates target-specific mossy fiber synapse development in the hippocampus

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
E Anne Martin ◽  
Shruti Muralidhar ◽  
Zhirong Wang ◽  
Diégo Cordero Cervantes ◽  
Raunak Basu ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Mossy Fiber ◽  
Neuron Activity ◽  
Target Cells ◽  
Synaptic Changes ◽  
Mossy Fiber Synapse ◽  
Ca3 Neurons ◽  
Circuit Function ◽  
Feed Forward Inhibition

Synaptic target specificity, whereby neurons make distinct types of synapses with different target cells, is critical for brain function, yet the mechanisms driving it are poorly understood. In this study, we demonstrate Kirrel3 regulates target-specific synapse formation at hippocampal mossy fiber (MF) synapses, which connect dentate granule (DG) neurons to both CA3 and GABAergic neurons. Here, we show Kirrel3 is required for formation of MF filopodia; the structures that give rise to DG-GABA synapses and that regulate feed-forward inhibition of CA3 neurons. Consequently, loss of Kirrel3 robustly increases CA3 neuron activity in developing mice. Alterations in the Kirrel3 gene are repeatedly associated with intellectual disabilities, but the role of Kirrel3 at synapses remained largely unknown. Our findings demonstrate that subtle synaptic changes during development impact circuit function and provide the first insight toward understanding the cellular basis of Kirrel3-dependent neurodevelopmental disorders.

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