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• W1986399413 abstract "Abstract S pinal m uscular a trophy is a genetic disease which severity depends on the amount of SMN protein, the product of the genes SMN 1 and SMN 2 . Symptomatology goes from severe neuromuscular impairment leading to early death in infants to slow progressing motor deficits during adulthood. Much of the knowledge about the pathophysiology of SMA comes from studies using genetically engineered animal models of the disease. Here we investigated one of the milder models, the homozygous A 2 G SMA mice, in which the level of the protein is restored to almost normal levels by the addition of a mutated transgene to the severe SMN ‐deficient background. We examined neuromuscular function and found that calcium‐dependent neurotransmitter release was significantly decreased. In addition, the amplitude of spontaneous endplate potentials was decreased, the morphology of NMJ altered, and slight changes in short‐term synaptic plasticity were found. In spite of these defects, excitation contraction coupling was well preserved, possibly due to the safety factor of this synapse. These data further support that the quasi‐normal restoration of SMN levels in severe cases preserves neuromuscular function, even when neurotransmitter release is significantly decreased at motor nerve terminals. Nevertheless, this deficit could represent a greater risk of motor impairment during aging or after injuries." @default.
• W1986399413 created "2016-06-24" @default.
• W1986399413 creator A5013291364 @default.
• W1986399413 creator A5075391736 @default.
• W1986399413 date "2013-03-13" @default.
• W1986399413 modified "2023-10-12" @default.
• W1986399413 title "Neurotransmitter release in motor nerve terminals of a mouse model of mild spinal muscular atrophy" @default.
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• W1986399413 doi "https://doi.org/10.1111/joa.12038" @default.
• W1986399413 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3867889" @default.
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