Journal
MATRIX BIOLOGY
Volume 57-58, Issue -, Pages 86-105Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.matbio.2016.08.008
Keywords
Aged; Bassoon; Neuromuscular junction; Laminin; Voltage-gated calcium channels
Categories
Funding
- National Institutes of Health [1R01NS078214, 1R01AG051470]
- National Institutes of Health K-INBRE postdoctoral award [P20 GM103418]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103418] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS078214] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG051470] Funding Source: NIH RePORTER
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The synapse between motor neurons and skeletal muscle is known as the neuromuscular junction (NMJ). Proper alignment of presynaptic and, post-synaptic structures of motor neurons and muscle fibers, respectively, is essential for efficient motor control of skeletal muscles. The synaptic cleft between these two cells is filled with basal lamina. Laminins are heterotrimer extracellular matrix molecules that are key members of the basal lamina. Laminin alpha 4, alpha 5, and beta 2 chains specifically localize to NMJs, and these laminin isoforms play a critical role in maintenance of NMJs and organization of synaptic vesicle release sites known as active zones. These individual laminin chains exert their role in organizing NMJs by binding to their receptors including integrins, dystroglycan, and voltage-gated calcium channels (VGCCs). Disruption of these laminins or the laminin-receptor interaction occurs in neuromuscular diseases including Pierson syndrome and Lambert Eaton myasthenic syndrome (LEMS). Interventions to maintain proper level of laminins and their receptor interactions may be insightful in treating neuromuscular diseases and aging related degeneration of NMJs. (C) 2016 Elsevier B.V. All rights reserved.
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