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1 nstant of repolarisation of the conditioning endplate potential.
2 s determined by micro-electrode recording of endplate potentials.
3 frequency but not the amplitude of miniature endplate potentials.
4 aracterized by a reduction in both miniature endplate potential amplitude and AChR abundance accompan
7 s muscle biopsy revealed decreased miniature endplate potential amplitudes, reduced endplate size and
8 t decrease of the amplitude of the miniature endplate potential and no deficiency of the ACh receptor
10 fatigable muscle weakness, reduced miniature endplate potentials and endplate potentials, reduced mot
11 el kinetics, or endplate ultrastructure, but endplate potentials depolarizing the resting potential t
12 or DuP 697, prevents the delayed increase in endplate potential (EPP) amplitude normally produced by
13 n the kinetics of stretch-induced changes in endplate potential (EPP) amplitude or miniature EPP (mEP
14 ontrol solution), the quantal content of the endplate potential (EPP) depressed more rapidly (approxi
15 nse to nerve stimulation was determined from endplate potentials (EPPs) and endplate currents (EPCs)
17 ality between staining/destaining and summed endplate potentials (EPPs) representing total transmitte
21 ological measurements of ACh secretion (i.e. endplate potentials, EPPs) and the component of the prej
22 ed acetylcholine (ACh) release (reflected as endplate potentials, EPPs) is well described by a simple
23 tosolic [Ca2+], and reduced the amplitude of endplate potentials evoked after the end of a stimulus t
24 oved synergistic in restoring suprathreshold endplate potentials in mouse diaphragms fully intoxicate
25 depressed nerve control, increased miniature endplate potential (MEPP) amplitude, decreased MEPP freq
26 monstrate an increased spontaneous miniature endplate potential (mEPP) frequency in Nedd4 mutants.
27 ncreases evoked quantal output and miniature endplate potential (MEPP) frequency, again by activating
29 measuring the relative changes of miniature endplate potentials (mEPPs) and voltage responses to ste
34 f spontaneous transmitter release (miniature endplate potentials (MEPPs)) from motor nerve terminals
36 tudy also showed a striking reduction of the endplate potential quantal content, consistent with addi
37 s, reduced miniature endplate potentials and endplate potentials, reduced motor endplate AChR number
39 ing continued, the fraction of the miniature endplate potential voltage-time integrals ( MEPPs) in th
40 the other hand, the mean amplitude of evoked endplate potentials was not decreased, due to an increas
41 The amplitude and rise time of miniature endplate potentials were also increased, but these chang
43 The amplitude and frequency of miniature endplate potentials were reduced, indicating impaired ne
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