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25-Hydroxycholesterol modulates synaptic vesicle endocytosis at the mouse neuromuscular junction.
Pflugers Arch
January 2025
Laboratory of Biophysics of Synaptic Processes, Kazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center of RAS, 2/31 Lobachevsky St, Kazan, 420111, RT, Russia.
Many synaptic vesicles undergo exocytosis in motor nerve terminals during neuromuscular communication. Endocytosis then recovers the synaptic vesicle pool and presynaptic membrane area. The kinetics of endocytosis may shape neuromuscular transmission, determining its long-term reliability.
View Article and Find Full Text PDFUsing Transcranial Magnetic Nerve Stimulation to Differentiate Motor and Sensory Fascicles in a Mixed Nerve: Experimental Rat Study.
J Reconstr Microsurg
January 2025
Department of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital, Taipei, Linkou, Chang Gung University, Taoyuan, Taiwan.
Background: Accurately matching the correct fascicles in a ruptured mixed nerve is critical for functional recovery. This study investigates the use of transcranial magnetic stimulation (TMS) to differentiate motor and sensory fascicles in a mixed nerve.
Methods: In all 40 rats, the median nerve in the left upper arm was evenly split into three segments.
An α7 nicotinic and GABA receptor-mediated pathway controls acetylcholine release in the tripartite neuromuscular junction.
J Physiol
December 2024
Université Paris Cité, CNRS, ENS Paris Saclay, Centre Borelli UMR 9010, Paris, France.
Terminal Schwann cells (TSCs) are capable of regulating acetylcholine (ACh) release at the neuromuscular junction (NMJ). We have identified GABA as a gliotransmitter at mouse NMJs. When ACh activates α7 nicotinic ACh receptor (nAChRs) on TSCs, GABA is released and activates GABA receptors on the nerve terminal that subsequently reduce ACh release.
View Article and Find Full Text PDFCompeting effects of activation history on force and cytosolic Ca in intact single mice myofibers.
Pflugers Arch
December 2024
School of Exercise and Nutritional Sciences, College of Health and Human Services, San Diego State University, 5500 Campanile Dr., San Diego, CA, 92182, USA.
The purpose was to investigate the changes in cytosolic Ca and force output during post-tetanic potentiation (PTP) during pre-fatigue and during prolonged low-frequency force depression (PLFFD) following fatigue. Intact single myofibers from the flexor digitorum brevis of mice were electrically stimulated to record force (n = 8) and free cytosolic Ca concentration ([Ca]) with FURA-2 (n = 6) at 32 °C. Initially, force and [Ca] were measured during brief (350 ms) trains of stimuli at 30, 50, 70, and 200 Hz at ~ 2 s intervals (Force-frequency protocol, FFP).
View Article and Find Full Text PDFIntrinsic Muscle Stem Cell Dysfunction Contributes to Impaired Regeneration in the mdx Mouse.
J Cachexia Sarcopenia Muscle
February 2025
Sprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Canada.
Background: Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
Methods: Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays.
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