ライフサイエンスコーパス: motor endplate

1 nchor the presynaptic fibers to the eventual motor endplate .

2 a diverse array of molecular targets at the motor endplate.

3 the nicotinic acetylcholine receptor at the motor endplate.

4 ansmission without overt degeneration of the motor endplate.

5 zed patch on the muscle membrane, termed the motor endplate.

6 COL13A1 localized to the human muscle motor endplate.

7 h AChRs at developing, adult, and denervated motor endplates.

8 ceptor, EphA8, localizes exclusively to fast motor endplates.

9 f regenerated nerve terminals still occupied motor endplates.

10 ynaptic strengths were co-regulated at these motor endplates.

11 r of the neuregulin family and is present at motor endplates.

12 ength and morphological deterioration of the motor endplates.

13 ohistochemistry revealed no abnormalities in motor endplates.

14 aused by abnormal signal transmission at the motor endplate, a special synaptic contact between motor

15 potentials and endplate potentials, reduced motor endplate AChR number and altered endplate morpholo

16 t observable AChR clusters at the developing motor endplate and that MuSK and AChRs codistribute thro

17 it and the defects that were observed in the motor endplates and muscles of the axJ mice.

18 how that ALG14 is concentrated at the muscle motor endplates and small interfering RNA silencing of A

19 yl transferase-like immunoreactive en plaque motor endplates and substance P-like immunoreactive, thi

20 Postsynaptic defects including increased motor endplate area and fragmentation were readily obser

21 No effects on motor endplate area or density were observed across trea

22 hR mRNA expression, muscle force production, motor endplate area, and innervation status.

23 ass after denervation, and reorganization of motor endplates at the postsynaptic sites compared with

24 can induced molecular reorganizations at the motor endplate, but the mechanism of action of agrin rem

25 damage to acetylcholine receptors (AChR) on motor endplates by autoantibody-induced complement attac

26 rget for therapeutic intervention to prevent motor endplate degradation following nerve injury.

27 he absence of Scn8a has been correlated with motor endplate disease (med), in which transient sodium

28 in the jolting mutant, a mild allele of the "motor endplate disease" locus.

29 We demonstrate that shrinkage of motor endplates does not correlate with loss of motor ne

30 target organ reinnervation is degradation of motor endplates during prolonged denervation.

31 Finally, severe degenerative changes at the motor endplate (endplate myopathy) were apparent by elec

32 ncentration of MuSK remains localized to the motor endplate even 14 days after denervation.

33 Motor endplates formed on the fibers derived from myobla

34 Analyses of motor endplates from two of the individuals demonstrate

35 t alpha-latrotoxin-like effect on the murine motor endplate, i.e. they bring about massive quantal re

36 While MuSK is normally restricted to the motor endplate in adult muscle, denervation results in i

37 oss of neuronal innervation and shrinkage of motor endplates in both diseases.

38 centrated at synaptic junctions in brain and motor endplates in skeletal muscle.

39 found that the extent of calcium overload of motor endplates in the panel of transgenic mice was infl

40 l but significant differences in variance of motor endplate length in motor units, which correlated w

41 g atrophy of muscle fibres and post-synaptic motor endplates, loss of lower motor neuron cell bodies

42 we report that synaptic terminals occupying motor endplates made electrically silent by tetrodotoxin

43 The polyneuronally innervated motor endplates (pi-junctions) were identified by vital

44 etylcholinesterase (AChE) molecular forms in motor endplate regions of adult Sprague-Dawley rat fast-

45 ilis muscle, as well as in the corresponding motor endplate regions where high levels of both AChE ac

46 ults demonstrate a critical role for MMP3 in motor endplate remodeling, and reveal a potential target

47 a receptor tyrosine kinase localized to the motor endplate, seemingly well positioned to receive a k

48 Pathologically, the motor endplates show focal accumulation of calcium and s

49 scle weight, fiber cross-sectional area, and motor endplate size and density.

50 it muscle mass, fiber oxidative capacity, or motor endplate size.

51 essive, asynchronous synapse withdrawal from motor endplates, strongly resembling neonatal synapse el

52 xtraocular muscles: those receiving a single motor endplate, termed singly innervated fibers (SIFs),

53 etrograde signaling mechanism located at the motor endplate that enables expression of adult motoneur

54 when acetylcholine receptors are blocked at motor endplates, the electrical properties of rat motone

55 ging experiments show calcium release at the motor endplate upon K+ depolarization precisely in these