Developmental neuromuscular synapse elimination: Activity-dependence and potential downstream effector mechanisms
1Department of Biology, Texas A&M University, College Station, TX, 77843, USA.
Neuroscience Letters
|December 27, 2019
Summary
During nervous system development, synapse elimination refines neural connections. This review explores how neuromuscular activity influences this critical process, impacting motor neuron and muscle fiber interactions.
Area of Science:
- Neuroscience
- Developmental Biology
- Synaptic Plasticity
Background:
- Synaptic connections undergo significant remodeling during nervous system maturation.
- Synapse elimination, where redundant presynaptic inputs are pruned, is crucial for proper neural function.
- Mammalian neuromuscular junctions serve as a key model for studying developmental synaptic remodeling.
Purpose of the Study:
- To review the contributions of motor neurons, synaptic glia, and muscle fibers to developmental synapse elimination.
- To explore the poorly understood downstream mechanisms by which neuromuscular activity influences synapse elimination.
- To investigate whether known cellular and molecular effectors of synapse elimination are modulated by neuromuscular activity.
Main Methods:
- This review synthesizes existing literature on synaptic development and elimination.
- It focuses on mechanisms at the mammalian neuromuscular junction.
- The review discusses cellular and molecular factors involved in synapse elimination.
Main Results:
- Neuromuscular activity is a primary driver of synapse elimination.
- Downstream signaling pathways linking neuromuscular activity to synapse elimination are not well-defined.
- The roles of motor neurons, glia, and muscle in this process are multifaceted.
Conclusions:
- Understanding how neuromuscular activity modulates the cellular and molecular players is key to deciphering synapse elimination.
- Further research is needed to elucidate the precise mechanisms involved.
- This process is essential for establishing functional neural circuits.
Related Concept Videos
The Neuromuscular Junction
17.5K
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...
17.5K
Neuromuscular Junction And Blockade
4.5K
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...
4.5K
Neurochemical Transmission: Sites of Drug Action
3.4K
Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
3.4K
Chemical Synapses
11.0K
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...
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...
11.0K
Chemical Synapses
4.1K
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...
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...
4.1K
Relaxation of Skeletal Muscles
5.4K
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....
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....
5.4K


