Dynamics of nerve-muscle interaction in developing and mature neuromuscular junctions

1995 ◽  
Vol 75 (4) ◽  
pp. 789-834 ◽  
Author(s):  
A. D. Grinnell
Keyword(s):  
Synapse Formation ◽  
Neuromuscular Junctions ◽  
Structure And Function ◽  
Axon Pathfinding ◽  
Control Of Gene Expression ◽  
Synaptic Structure ◽  
Dynamic Cell ◽  
Nerve Muscle ◽  
And Function ◽  
Motoneuron Cell

Neuromuscular connections have long served as models of synaptic structure and function. They also provide illuminating insights into the dynamic cell-cell interactions governing synaptogenesis, neuromuscular differentiation, and the maintenance of effective function. This paper reviews recent advances in our understanding of the regulatory and inductive interactions involved in motor axon pathfinding, target recognition, bidirectional control of gene expression during synapse formation, motoneuron cell death, terminal rearrangement, and the ongoing remodeling of synaptic number, structure, and function to adjust to growth and changes in use.

scholarly journals Regulation of synaptic structure and function by palmitoylated AMPA receptor binding protein

2010 ◽  
Vol 43 (4) ◽  
pp. 341-352 ◽  
Author(s):  
Charu Misra ◽  
Sophie Restituito ◽  
Jainne Ferreira ◽  
Gerald A. Rameau ◽  
Jie Fu ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Receptor Binding ◽  
Binding Protein ◽  
Structure And Function ◽  
Synaptic Structure ◽  
Ampa Receptor Binding Protein ◽  
And Function ◽  
Receptor Binding Protein

scholarly journals Genetic Analysis of Collagen Q: Roles in Acetylcholinesterase and Butyrylcholinesterase Assembly and in Synaptic Structure and Function

1999 ◽  
Vol 144 (6) ◽  
pp. 1349-1360 ◽  
Author(s):  
Guoping Feng ◽  
Eric Krejci ◽  
Jordi Molgo ◽  
Jeanette M. Cunningham ◽  
Jean Massoulié ◽  
...  
Keyword(s):  
Neuromuscular Junctions ◽  
Synaptic Cleft ◽  
Neuromuscular Function ◽  
Nerve Terminals ◽  
Compensatory Mechanisms ◽  
Structural Mechanism ◽  
Synaptic Structure ◽  
Cardiac Muscles ◽  
And Function ◽  
Early Phases

Acetylcholinesterase (AChE) occurs in both asymmetric forms, covalently associated with a collagenous subunit called Q (ColQ), and globular forms that may be either soluble or membrane associated. At the skeletal neuromuscular junction, asymmetric AChE is anchored to the basal lamina of the synaptic cleft, where it hydrolyzes acetylcholine to terminate synaptic transmission. AChE has also been hypothesized to play developmental roles in the nervous system, and ColQ is also expressed in some AChE-poor tissues. To seek roles of ColQ and AChE at synapses and elsewhere, we generated ColQ-deficient mutant mice. ColQ−/− mice completely lacked asymmetric AChE in skeletal and cardiac muscles and brain; they also lacked asymmetric forms of the AChE homologue, butyrylcholinesterase. Thus, products of the ColQ gene are required for assembly of all detectable asymmetric AChE and butyrylcholinesterase. Surprisingly, globular AChE tetramers were also absent from neonatal ColQ−/− muscles, suggesting a role for the ColQ gene in assembly or stabilization of AChE forms that do not themselves contain a collagenous subunit. Histochemical, immunohistochemical, toxicological, and electrophysiological assays all indicated absence of AChE at ColQ−/− neuromuscular junctions. Nonetheless, neuromuscular function was initially robust, demonstrating that AChE and ColQ do not play obligatory roles in early phases of synaptogenesis. Moreover, because acute inhibition of synaptic AChE is fatal to normal animals, there must be compensatory mechanisms in the mutant that allow the synapse to function in the chronic absence of AChE. One structural mechanism appears to be a partial ensheathment of nerve terminals by Schwann cells. Compensation was incomplete, however, as animals lacking ColQ and synaptic AChE failed to thrive and most died before they reached maturity.

STRUCTURE AND FUNCTION OF NEUROMUSCULAR JUNCTIONS IN THE VASTUS LATERALIS OF MAN

Brain ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 451-478 ◽  
Author(s):  
E. BOLLEN ◽  
J. C. DEN HEYER ◽  
M. H. J. TOLSMA ◽  
S. BELLAR ◽  
J. E. BOS ◽  
...  
Keyword(s):  
Neuromuscular Junctions ◽  
Vastus Lateralis ◽  
Structure And Function ◽  
And Function

Consequences of Pharmacological BACE Inhibition on Synaptic Structure and Function

2018 ◽  
Vol 84 (7) ◽  
pp. 478-487 ◽  
Author(s):  
Kaichuan Zhu ◽  
Finn Peters ◽  
Severin Filser ◽  
Jochen Herms
Keyword(s):  
Structure And Function ◽  
Synaptic Structure ◽  
And Function

Synaptopathy: dysfunction of synaptic function?

2010 ◽  
Vol 38 (2) ◽  
pp. 443-444 ◽  
Author(s):  
Nils Brose ◽  
Vincent O'Connor ◽  
Paul Skehel
Keyword(s):  
Animal Experimentation ◽  
Structure And Function ◽  
Synaptic Function ◽  
Cellular Systems ◽  
Brain Diseases ◽  
Psychiatric Disease ◽  
Synaptic Dysfunction ◽  
A Value ◽  
Synaptic Structure ◽  
And Function

Synaptopathy is an increasingly popular term used to define key features of neurodegenerative and psychiatric disease. It implies that disruptions in synaptic structure and function are potentially the major determinant of such brain diseases. The Synaptopathies: Dysfunction of Synaptic Function Biochemical Society Focused Meeting brought together several invited speakers, supplemented with short communications from young scientists, who addressed this possibility. The talks spanned the full gamut of approaches that brought molecular, cellular, systems and whole-animal experimentation together to address how fundamental synaptic biology was increasingly informing on dysfunction in disease. The disease and models thereof discussed included Alzheimer's disease, prions, Huntington's disease, Parkinson's disease, schizophrenia and autism. The audience were asked to reflect on whether synaptopathy, although attractive and conceptually useful, provided a significant explanation as the cause of these major diseases. The breadth of the meeting reinforced the complexity of these brain diseases, supported the significance of synaptic dysfunction in disease, but left open the issue as to whether the prime cause of these disorders could be resolved as simple synaptic dysfunction. Thus, despite revealing a value of synaptopathy, further investigation will be required to reveal its balance in the cause and effect in each of the major brain diseases.

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.

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