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Ryanodine and inositol triphosphate receptors modulate facilitation and tetanic depression at the frog neuromuscular junction
Author(s) -
Silveira Priscila E.,
Lima Ricardo F.,
GuimarÃES Jennifer D.S.,
Molgó Jordi,
Naves Ligia A.,
Kushmerick Christopher
Publication year - 2015
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.24571
Subject(s) - ryanodine receptor , neuromuscular junction , biology , inositol , neuromuscular transmission , medicine , endocrinology , neuroscience , receptor , biochemistry
Short‐term plasticity of synaptic function is an important physiological control of transmitter release. Short‐term plasticity can be regulated by intracellular calcium released by ryanodine and inositol triphosphate (IP3) receptors, but the role of these receptors at the neuromuscular junction is understood incompletely. Methods We measured short‐term plasticity of evoked endplate potential (EPP) amplitudes from frog neuromuscular junctions treated with ryanodine, 2‐aminoethoxydiphenylborane (2‐APB), or 1‐[6‐[[(17β)‐3‐methoxyestra‐1,3,5(10)‐trien‐17‐yl]amino]hexyl]‐1H‐pyrrole‐2,5‐dione (U‐ 73122). Results Ryanodine decreases paired‐pulse facilitation for intervals <20 ms and markedly decreases tetanic depression. Treatment with 2‐APB reduces EPP amplitude, increases paired‐pulse facilitation for intervals of <20 ms, and significantly reduces tetanic depression. U‐73122 decreases EPP amplitude and decreases paired‐pulse depression for intervals <20 ms. Conclusions Ryanodine, IP3 receptors, and phopholipase C modulate short‐term plasticity of transmitter release at the neuromuscular junction. These results suggest possible targets for improving the safety factor of neuromuscular transmission during repetitive activity of the neuromuscular junction. Muscle Nerve 52: 623–630, 2015