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Updated: Jun 3, 2026

Physiological Recordings of High and Low Output NMJs on the Crayfish Leg Extensor Muscle
Published on: November 17, 2010
Neuromuscular synaptic patterning requires the function of skeletal muscle dihydropyridine receptors
Fujun Chen1, Yun Liu, Yoshie Sugiura
1Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Abstract:
Developing skeletal myofibers in vertebrates are intrinsically 'pre-patterned' for motor nerve innervation. However, the intrinsic factors that regulate muscle pre-patterning remain unknown. We found that a functional skeletal muscle dihydropyridine receptor (DHPR, the L-type Ca(2+) channel in muscle) was required for muscle pre-patterning during the development of the neuromuscular junction (NMJ). Targeted deletion of the β1 subunit of DHPR (Cacnb1) in mice led to muscle pre-patterning defects, aberrant innervation and precocious maturation of the NMJ. Reintroducing Cacnb1 into Cacnb1(-/-) muscles reversed the pre-patterning defects and restored normal development of the NMJ. The mechanism by which DHPRs govern muscle pre-patterning is independent of their role in excitation-contraction coupling, but requires Ca(2+) influx through the L-type Ca(2+) channel. Our findings indicate that the skeletal muscle DHPR retrogradely regulates the patterning and formation of the NMJ.
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