Abstract：
:Neurotrophins and tyrosine receptor kinase (Trk) receptors are expressed in skeletal muscle, but it is unclear what functional role Trk-mediated signaling plays during postnatal life. Full-length TrkB (trkB.FL) as well as truncated TrkB (trkB.t1) were found to be localized primarily to the postsynaptic acetylcholine receptor- (AChR-) rich membrane at neuromuscular junctions. In vivo, dominant-negative manipulation of TrkB signaling using adenovirus to overexpress trkB.t1 in mouse sternomastoid muscle fibers resulted in the disassembly of postsynaptic AChR clusters at neuromuscular junctions, similar to that observed in mutant trkB+/- mice. When TrkB-mediated signaling was disrupted in cultured myotubes in the absence of motor nerve terminals and Schwann cells, agrin-induced AChR clusters were also disassembled. These results demonstrate a novel role for neurotrophin signaling through TrkB receptors on muscle fibers in the ongoing maintenance of postsynaptic AChR regions.
journal_name
Neuronjournal_title
Neuronauthors
Gonzalez M,Ruggiero FP,Chang Q,Shi YJ,Rich MM,Kraner S,Balice-Gordon RJdoi
10.1016/s0896-6273(00)81113-7subject
Has Abstractpub_date
1999-11-01 00:00:00pages
567-83issue
3eissn
0896-6273issn
1097-4199pii
S0896-6273(00)81113-7journal_volume
24pub_type
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