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Related Concept Videos

The Neuromuscular Junction01:19

The Neuromuscular Junction

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...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

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...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

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.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Electrical Synapses01:28

Electrical Synapses

Electrical synapses found in all nervous systems play important and unique roles. In these synapses, the presynaptic and postsynaptic membranes are very close together (3.5 nm) and are actually physically connected by channel proteins forming gap junctions.
Gap junctions allow the current to pass directly from one cell to the next. In contrast, in the chemical synapse, the neurotransmitters carry the information through the synaptic cleft from one neuron to the next. They consist of two...

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Related Experiment Video

Updated: Jun 8, 2026

The Neuromuscular Junction: Measuring Synapse Size, Fragmentation and Changes in Synaptic Protein Density Using Confocal Fluorescence Microscopy
12:18

The Neuromuscular Junction: Measuring Synapse Size, Fragmentation and Changes in Synaptic Protein Density Using Confocal Fluorescence Microscopy

Published on: December 26, 2014

Silent synapses in neuromuscular junction development.

Josep Tomàs1, Manel M Santafé, Maria A Lanuza

  • 1Unitat d'Histologia i Neurobiologia (UHN), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Reus, Spain. jmtf@fmcs.urv.es

Journal of Neuroscience Research
|September 22, 2010
PubMed
Summary

Silent synapses can be reactivated during muscle development. A proposed mechanism involves protein kinase C (PKC) inhibiting acetylcholine (ACh) release, balanced by brain-derived neurotrophic factor (BDNF) signaling.

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Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures
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Characterization of Neuromuscular Junctions in Mice by Combined Confocal and Super-Resolution Microscopy
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Characterization of Neuromuscular Junctions in Mice by Combined Confocal and Super-Resolution Microscopy

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Last Updated: Jun 8, 2026

The Neuromuscular Junction: Measuring Synapse Size, Fragmentation and Changes in Synaptic Protein Density Using Confocal Fluorescence Microscopy
12:18

The Neuromuscular Junction: Measuring Synapse Size, Fragmentation and Changes in Synaptic Protein Density Using Confocal Fluorescence Microscopy

Published on: December 26, 2014

Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures
08:13

Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures

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Characterization of Neuromuscular Junctions in Mice by Combined Confocal and Super-Resolution Microscopy
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Characterization of Neuromuscular Junctions in Mice by Combined Confocal and Super-Resolution Microscopy

Published on: December 8, 2021

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Molecular Biology

Background:

  • During postnatal development, neuromuscular synapses undergo elimination, a process where some synapses become silent before complete retraction.
  • Understanding the mechanisms behind synapse silencing and potential reactivation is crucial for comprehending neural development and plasticity.

Purpose of the Study:

  • To propose a molecular mechanism for axonal disconnection during developmental synapse elimination.
  • To elucidate the roles of protein kinase C (PKC), muscarinic receptors, and neurotrophic factors in regulating neuromuscular synapse function.

Main Methods:

  • This mini-review synthesizes existing published data and incorporates new findings.
  • The proposed mechanism focuses on the regulation of acetylcholine (ACh) release via PKC signaling pathways.

Main Results:

  • A proposed mechanism involves protein kinase C (PKC)-dependent inhibition of acetylcholine (ACh) release.
  • PKC activity is potentially stimulated by methoctramine-sensitive M2-type muscarinic receptors and calcium influx via P/Q- and L-type channels.
  • Tropomyosin-related tyrosine kinase B (trkB) receptor-mediated brain-derived neurotrophic factor (BDNF) activity may counteract PKC-induced ACh release inhibition.

Conclusions:

  • A balance between trkB and muscarinic signaling pathways may determine the final functional suppression of neuromuscular synapses during development.
  • This molecular interplay offers insights into the dynamic regulation of synapse elimination and potential for functional recovery.