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Related Concept Videos

The Neuromuscular Junction01:19

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The nervous system consists of complex motor neuron circuits, including upper motor neurons originating from the cerebral cortex and lower motor neurons starting in the spinal cord, coordinating both voluntary and involuntary movements. Among these, somatic motor neurons activate skeletal muscles and are classified into alpha, beta, and gamma types. Alpha neurons are vital for voluntary movement coordination, while gamma neurons adjust muscle spindle sensitivity, and the function of beta...
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The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
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The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
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As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
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Skeletal muscle cells, also called muscle fibers, are distinctly elongated, multi-nucleated, slender biological units. They are packed with specialized structures designed to facilitate their primary function, which is contraction.
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Every cell in the body maintains a membrane potential due to an uneven distribution of positive and negative charges across its plasma membrane. The membrane potential is measured in millivolts and quantifies the difference in charge across the membrane.
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Updated: Sep 8, 2025

Dissection of Single Skeletal Muscle Fibers for Immunofluorescent and Morphometric Analyses of Whole-Mount Neuromuscular Junctions
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LSMEM2, Localized at the Neuromuscular Junction, Modulates Mitochondrial Integration in Skeletal Muscles.

Eman Elrefaei1,2,3, Satoru Yamazaki1, Issei Yazawa1

  • 1Department of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 17, 2025
PubMed
Summary
This summary is machine-generated.

Adenosine monophosphate-activated protein kinase (AMPK) substrate LSMEM2 is found at the neuromuscular junction. LSMEM2 overexpression in male mice causes skeletal muscle abnormalities, suggesting a role in muscle disease pathogenesis.

Keywords:
intercalated disc (ICD)membrane proteinneuromuscular junction (NMJ)skeletal muscle diseasessubsarcolemmal mitochondriatubular aggregate

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Muscle Physiology

Background:

  • Adenosine monophosphate-activated protein kinase (AMPK) has canonical and noncanonical functions, including substrate phosphorylation.
  • LSMEM2, a novel AMPK substrate, is a membrane protein identified in the heart and expressed in skeletal muscles.

Purpose of the Study:

  • To investigate the role and function of LSMEM2 in skeletal muscles.
  • To determine the consequences of LSMEM2 absence or overexpression in skeletal muscle.

Main Methods:

  • Utilized LSMEM2-knockout mice to assess development and histology.
  • Overexpressed LSMEM2 in male mice and analyzed skeletal muscle phenotype.
  • Performed RNA sequencing to identify enriched gene sets.
  • Conducted histological analysis of muscle tissue.

Main Results:

  • LSMEM2 is localized at the neuromuscular junction (NMJ) in skeletal muscle.
  • LSMEM2 knockout mice showed no developmental abnormalities.
  • Skeletal muscle overexpression of LSMEM2 led to tubular aggregate formation and functional deficits in male mice.
  • Gene expression analysis revealed enrichment in mitochondrial oxidative phosphorylation and vesicle-mediated transport pathways.
  • Histology showed swollen subsarcolemmal mitochondria accumulation in LSMEM2-overexpressing muscles.

Conclusions:

  • LSMEM2 is not essential for skeletal muscle development.
  • LSMEM2 overexpression induces skeletal muscle pathology, including mitochondrial dysfunction.
  • LSMEM2 may contribute to the pathogenesis of skeletal muscle diseases.