Investigating the safety factor at an invertebrate neuromuscular junction

Fidelity of synaptic transmission is essential at the neuromuscular junction (NMJ). To ensure that transmission does not fail, vertebrate motoneurons often release more neurotransmitter than is required for muscle contraction. This safety factor allows some loss of synaptic function without failure...

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Published inJournal of neurobiology Vol. 63; no. 1; p. 62
Main Authors Marrus, Scott B, DiAntonio, Aaron
Format Journal Article
LanguageEnglish
Published United States 01.04.2005
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Abstract Fidelity of synaptic transmission is essential at the neuromuscular junction (NMJ). To ensure that transmission does not fail, vertebrate motoneurons often release more neurotransmitter than is required for muscle contraction. This safety factor allows some loss of synaptic function without failure of muscle contraction. It is not known whether a similar mechanism operates at the invertebrate neuromuscular junction. In our study of the Drosophila NMJ, we find that glutamate receptor mutants can exhibit a substantial decrease in synaptic function while maintaining muscle contraction. The persistence of neuromuscular function in these mutants is not explained by synaptic facilitation, temporal summation of high frequency stimuli, or a hyperpolarizing shift in the activation range of muscle calcium channels. Instead, the attenuated synaptic response is sufficient to drive muscle contraction. Quantitative analysis of the decrease in synaptic transmission in these mutants implies that at the wild-type NMJ there is an approximately five- to ninefold excess in released transmitter. Hence, the presence of a synaptic safety factor is a conserved feature of neuromuscular organization in both invertebrates and vertebrates.
AbstractList Fidelity of synaptic transmission is essential at the neuromuscular junction (NMJ). To ensure that transmission does not fail, vertebrate motoneurons often release more neurotransmitter than is required for muscle contraction. This safety factor allows some loss of synaptic function without failure of muscle contraction. It is not known whether a similar mechanism operates at the invertebrate neuromuscular junction. In our study of the Drosophila NMJ, we find that glutamate receptor mutants can exhibit a substantial decrease in synaptic function while maintaining muscle contraction. The persistence of neuromuscular function in these mutants is not explained by synaptic facilitation, temporal summation of high frequency stimuli, or a hyperpolarizing shift in the activation range of muscle calcium channels. Instead, the attenuated synaptic response is sufficient to drive muscle contraction. Quantitative analysis of the decrease in synaptic transmission in these mutants implies that at the wild-type NMJ there is an approximately five- to ninefold excess in released transmitter. Hence, the presence of a synaptic safety factor is a conserved feature of neuromuscular organization in both invertebrates and vertebrates.
Author DiAntonio, Aaron
Marrus, Scott B
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Snippet Fidelity of synaptic transmission is essential at the neuromuscular junction (NMJ). To ensure that transmission does not fail, vertebrate motoneurons often...
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StartPage 62
SubjectTerms Action Potentials - genetics
Action Potentials - radiation effects
Animals
Animals, Genetically Modified
Calcium - metabolism
Drosophila
Drosophila Proteins - deficiency
Drosophila Proteins - genetics
Electric Stimulation - methods
Female
In Vitro Techniques
Invertebrates
Larva - physiology
Membrane Potentials - physiology
Membrane Potentials - radiation effects
Muscle Contraction - physiology
Muscle Contraction - radiation effects
Neural Inhibition - genetics
Neural Inhibition - radiation effects
Neuromuscular Junction - physiology
Neuromuscular Junction - radiation effects
Neurotransmitter Agents - metabolism
Patch-Clamp Techniques - methods
Receptors, Glutamate - deficiency
Receptors, Glutamate - genetics
Synaptic Transmission - physiology
Title Investigating the safety factor at an invertebrate neuromuscular junction
URI https://www.ncbi.nlm.nih.gov/pubmed/15685612
Volume 63
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