ライフサイエンスコーパス: end plate

1 fluence removal of excess innervation at the end plate.

2 omposition depends on the orientation of the end plate.

3 splaying acetylcholinesterase-positive motor end plates.

4 from C6 were the sole input to reinnervated end plates.

5 there are morphological changes at the motor end-plates.

6 ease in gamma-subunit mRNA expression at CMS end-plates.

7 silon, delta, beta and alpha subunits of the end plate acetylcholine (ACh) receptor (AChR) are descri

8 ain of function mutations in subunits of the end-plate acetylcholine receptor (AChR).

9 Congenital end-plate acetylcholinesterase (AChE) deficiency (CEAD),

10 Human end-plate AChE deficiency was recently shown to be cause

11 nine novel COLQ mutations in 7 patients with end-plate AChE deficiency.

12 on of the foetal-specific gamma-subunit into end-plate AChR.

13 d by the binding of complement-fixing IgG to end-plate AChRs.

14 nded on accurate identification of vertebral end plates and posterior elements.

15 , 57, and 66 years) containing cartilaginous end plates and subchondral bone were prepared.

16 in areas surrounding the nuclei of the motor end plate, and in perisynaptic Schwann cells, and locali

17 occurs across the fibrous capsule around the end plate, and the major determinants of the final intra

18 on may be achieved with implants with larger end plates, and valved implants appear to reduce the ris

19 Samples were imaged with the end plate at three orientations with respect to the cons

20 c neuregulin expression and maintains normal end plate band architecture in the presence of activity

21 synaptic differentiation and formation of an end-plate band require MuSK and rapsyn, but are not depe

22 , or why most synapses are restricted to an 'end-plate band' in the middle of the muscle remains unkn

23 When end-plate border properties of fibers from 3 MG patients

24 At the end-plate border we examined miniature end-plate potenti

25 evels of mRNA for AChR subunits at the motor end-plates by in situ hybridization.

26 d in articular cartilage from older mice, in end-plate cartilage from mice, and in chondrocytes from

27 growth and/or a fall in blood supply through end plate changes could instigate NC disappearance.

28 ransition from C7- to C6-dominated input, at end plates coinnervated by C6 and C7 axons, the average

29 udies demonstrated that changes in the inlet end plate configuration designed to ensure uniform flow

30 second denervation, most of the reinnervated end plates contained only axons from the C7 branch; the

31 End plate current simulations suggest that the higher af

32 ure end-plate potential (MEPP) and miniature end-plate current (MEPC); at 5 x 10(-3) M, the MEPP beca

33 All three had prolonged end plate currents and AChR channel opening episodes and

34 er, the quantal size (amplitude of miniature end-plate currents) and the kinetic properties of synapt

35 s a hitherto unrecognized consequence of the end-plate damage initiated by the binding of complement-

36 ons in the nicotinic receptor from the motor end plate decreases unitary conductance up to 80%.

37 eaching experiments carried out a frog motor end-plates demonstrated lack of lateral intermixing of s

38 Motor end plates denervated by axonal retraction of dying moto

39 by MRI, including Romanus lesions (RLs) and end-plate, diffuse vertebral body, posterior element, an

40 nels is associated with the phenotype "motor end plate disease," which is characterized by a progress

41 parameters, like ESI voltage and ESI tip-to-end plate distance, were optimized for very low flow rat

42 End-plate edema, degenerative discs, and RLs were freque

43 unrelated patients with very small miniature end plate (EP) potentials, but with normal EP AChR densi

44 l myasthenic syndrome associated with severe end-plate (EP) acetylcholine receptor (AChR) deficiency

45 d quantitative electron microscopy EM of 409 end plates (EPs), and by mutation analysis, and expressi

46 ion of the degeneration of the cartilaginous end plate; however, the accuracy of T2*-based estimates

47 s of voltage-gated Na+ channels at the motor end plate in both patients with MG and in rats with PTMG

48 vidence of more degeneration of the disc and end plate in the spines of Col9a1(-/-) mice compared wit

49 Amplitudes of MEPPs and INa at the end plate indicated that loss of AChRs was greater than

50 ter 6 d, the pattern was reversed, with most end plates innervated exclusively by C6.

51 Classic signs include vertebral end plate irregularity, disk space narrowing, and anteri

52 cases a destruction of vertebral bodies with end plates loss restriction and cortical layer discontin

53 rately positioned using holes drilled in two end plates made of plastic.

54 Reelin is required for motor end-plate maturation and proper nerve-muscle connectivit

55 The end plate myopathy stems from cationic overloading of th

56 nts and AChR channel opening episodes and an end plate myopathy with loss of AChR from degenerating j

57 el, leading to a depolarization block and an end-plate myopathy.

58 Compared with WT mice, motor end-plates of mdx mice demonstrated less continuous morp

59 ssion of alpha- and epsilon-subunit mRNAs at end-plates of patient and control muscles, suggesting th

60 Higher end plate porosity in discs with NCs suggested greater n

61 used scanning electron microscopy to examine end plate porosity of discs with NCs and those with MNPC

62 not after a tetanus, increased the speed of end plate potential (EPP) amplitude rundown, and greatly

63 End plate potential (EPP) amplitudes were used to follow

64 ionally, miniature end plate potential size, end plate potential size, and quantal content did not di

65 Functionally, miniature end plate potential size, end plate potential size, and

66 plitude and decay time constant of miniature end-plate potential (MEPP) and miniature end-plate curre

67 loroquine reduced the quantal content of the end-plate potential by 37-45%.

68 ock owing to temporal summation of prolonged end plate potentials at physiologic rates of stimulation

69 End-plate potentials (EPPs) and miniature end-plate pote

70 as the frequency of occurrence of miniature end-plate potentials (MEPP(f)), were evoked by high pota

71 Miniature end-plate potentials (MEPPs) were focally recorded from

72 End-plate potentials (EPPs) and miniature end-plate potentials (MEPPs) were recorded from neuromus

73 t the end-plate border we examined miniature end-plate potentials (MEPPs), sodium current (INa) ampli

74 ed to 10-30% of normal levels, the miniature end-plate potentials are correspondingly reduced, and th

75 ronous ACh release evoked by nerve impulses (end-plate potentials, EPPs) follow a simple binomial dis

76 om the C7 branch; the remaining reinnervated end plates received input from C6 only or were multiply

77 <0.01) and at 12 months (P<0.10) and for the end plate region only at 6 months (P<0.10).

78 as acetylcholine receptors (AChRs) from the end-plate region in patients with acquired myasthenia gr

79 cence and ultrastructural analyses of muscle end-plate regions showed synaptic remodelling with dener

80 ed; rather, it resulted from a lack of motor end plate reinnervation.

81 tween CAV-1 and alphaC418W that could confer end plates rich in alphaC418W nAChRs to a susceptibility

82 Larger end-plate size is associated with greater intraocular pr

83 The end-plate species of acetylcholinesterase (AChE) is an a

84 Degeneration in the end plates was associated with more cell proliferation,

85 End plates were 14% smaller in N-CAM-deficient mice than

86 Smaller axons and motor end plates were also demonstrated in SM, using NADPH-dia

87 omical analysis indicated that 50% of soleus end plates were completely denervated 1-4 weeks post-par

88 nsmission is ensured by the large INa at the end plate, which reduces the AP threshold.

89 ntering through an aperture in the dc-biased end plate, which was also operated as an ion gate.

90 ion showed thickened bone in the Cupid's bow end plate with annular fibers inserting into this region

91 Axons terminating in motor end plates within SM bundles were immunoreactive to PHA-