ライフサイエンスコーパス: motor nerve

1 he medial plantar nerve, a mixed sensory and motor nerve.

2 response to a single stimulus applied to the motor nerve.

3 and there is a subsequent loss of the facial motor nerve.

4 oduce identical phenotypes affecting the SNa motor nerve.

5 lar nuclei, and the nuclei of the trigeminal motor nerves.

6 mice studies of large myelinated sensory and motor nerves.

7 rior rectus EOMs and small or absent orbital motor nerves.

8 entials evoked by stimulating postganglionic motor nerves.

9 lectrodes were placed bilaterally on the SNB motor nerves.

10 or forming and maintaining functional spinal motor nerves.

11 es the basis for the organisation of cranial motor nerves.

12 st unchanged even after damage to downstream motor nerves.

13 isions made by axons within the ISN and ISNb motor nerves.

14 s and instead continue to extend along their motor nerves.

15 by the interaction between muscle fibres and motor nerves.

16 gh the slow component was negligible in some motor nerves.

17 sting potential in sensory and at least some motor nerves.

18 nin gene-related peptide (CGRP) from sensory-motor nerves.

19 leading to immune-mediated injury of distal motor nerves.

20 expression was also able to generate ectopic motor nerves.

21 s, deficient supraduction, and small orbital motor nerves.

22 Stimulating the inferior gluteal motor nerve (0.1 ms pulse, 100 Hz for 500 ms) evoked a b

23 letal muscle adapts to different patterns of motor nerve activity by alterations in gene expression t

24 Different patterns of motor nerve activity drive distinctive programs of gene

25 ion, we recorded ipsi- and contralateral SNB motor nerve activity following unilateral spinal stimula

26 Recently, we proposed that the influence of motor nerve activity on skeletal muscle fiber type is tr

27 lar mechanism by which different patterns of motor nerve activity promote selective changes in gene e

28 ved to increase mechanical stability and the motor nerve activity served as a surrogate for muscle fo

29 quantitatively similar increases in efferent motor nerve activity to protrudor and retractor tongue m

30 legs maintained constant posture without leg motor nerve activity when the animals were rotated in ai

31 epletion resulted in decreased amplitudes of motor nerve activity, and these changes were attenuated

32 mediates key responses of skeletal muscle to motor nerve activity.

33 ealed striking signs of hyperexcitability in motor nerves after oxaliplatin.

34 Each muscle region is supplied by its own motor nerve and feed artery with an anastomotic arteriol

35 s in the laminin-alpha2 gene, and results in motor nerve and skeletal muscle dysfunction.

36 ne as essential for motor axons to leave the motor nerves and enter their muscle targets.

37 hat neuropeptides are present in the lateral motor nerves and in nerve processes innervating inteross

38 llular interactions between laser transected motor nerves and macrophages in live intact zebrafish.

39 lped distinguish different components of the motor nerves and neuromuscular junction.

40 axons defasciculate from other axons in the motor nerves and steer into their muscle target regions.

41 ies were concentrated in varicose regions of motor nerves and were closely apposed to ICC-IM but not

42 lude defasciculation and degeneration of the motor nerves, and an absence of Schwann cells.

43 with bilateral abnormalities of many orbital motor nerves, and structural abnormalities of all EOMs e

44 ether to produce segmentation of sensory and motor nerves, and that dorsal peripheral nervous system

45 Consistent segregation of intramuscular motor nerve arborization suggests functionally distinct

46 Later developing secondary motor nerves are also delayed in entering the ventral my

47 es, during adult fictive limb-kicking, these motor nerves are synchronously active in accordance with

48 ncreased following injury or degeneration of motor nerves, as a process to mitigate neurogenic muscle

49 in sympathetic, parasympathetic, and sensory-motor nerves, as well as in intracardiac neurons.

50 isoform of MFas II (GPI-MFas II) labeled the motor nerves at all stages and seemed to be associated w

51 After facial motor nerve axotomy, dramatic changes in the levels of C

52 vivo, that nodes of Ranvier in intramuscular motor nerve bundles are also targeted by anti-GD1a antib

53 ine inhibits neurotransmitter secretion from motor nerves by an effect on the secretory apparatus in

54 During synaptogenesis, agrin, released by motor nerves, causes the clustering of acetylcholine rec

55 lded unique activity patterns in extraocular motor nerves, compatible with a spatially and temporally

56 nerve blood flow (NBF) vs. other factors in motor nerve conduction (MNC) slowing in short-term diabe

57 Patients were classified into five groups by motor nerve conduction criteria; 69% were demyelinating,

58 y nerve conduction deficit without affecting motor nerve conduction slowing.

59 educed voluntary locomotor activity, reduced motor nerve conduction velocities (MNCVs) and muscle atr

60 mise, a markedly low birth weight, very slow motor nerve conduction velocities and a general decrease

61 e analyses also reveal that the reduction of motor nerve conduction velocities in affected patients i

62 Motor nerve conduction velocities of the fastest fibers

63 Motor nerve conduction velocities showed normal values (

64 on age of onset and the degree of slowing of motor nerve conduction velocities.

65 ndent vascular relaxation precede slowing of motor nerve conduction velocity (MNCV) and decreased sci

66 eeks old) clearly developed manifest sciatic motor nerve conduction velocity (MNCV) and hind-limb dig

67 ation and axonal loss, which underlie slowed motor nerve conduction velocity (MNCV) and reduced compo

68 Endoneurial blood flow and motor nerve conduction velocity (MNCV) were impaired in

69 diabetic with streptozotocin, and changes in motor nerve conduction velocity (MNCV), mechanical and t

70 ological abnormalities of EDN, i.e., reduced motor nerve conduction velocity (MNCV), total and endone

71 zed diabetes-induced deficits in sensory and motor nerve conduction velocity (P < 0.05).

72 Peroneal motor nerve conduction velocity (p=0.03) and M-wave ampl

73 d po), it normalizes polyols and reduces the motor nerve conduction velocity deficit by 59% relative

74 Composite motor nerve conduction velocity for the median, ulnar, a

75 Polyol content was elevated (P < 0.001) and motor nerve conduction velocity reduced (P < 0.05) in ga

76 t both (R/S)-1 and (R)-1 partially prevented motor nerve conduction velocity slowing in a mouse model

77 Upper limb motor nerve conduction velocity was 19.9 m/s +/- 1.3 (SE

78 Motor nerve conduction velocity was moderately reduced i

79 Sciatic motor nerve conduction velocity, hindlimb digital sensor

80 physiological evaluation of both sensory and motor nerve conduction was performed.

81 eatine kinase, muscle strength and function, motor nerve conduction, activities of daily living, and

82 tudies showed normal large fibre sensory and motor nerve conduction; however, skin biopsy showed a si

83 d hind limb digital sensory, but not sciatic motor, nerve conduction slowing and thermal and mechanic

84 d vascular relationships of the three ocular motor nerves (cranial nerves III, IV, and VI) and of the

85 ons to their target muscles on schedule, but motor nerves defasciculate upon reaching the muscle surf

86 timeters-long portions of these axons in the motor nerves depolarize in response to low concentration

87 ining showed similar binding to sensory- and motor nerve-derived GD1a in a solid phase assay, we gene

88 uch as perineurial glia, properly encase the motor nerve despite this change in glial cell and myelin

89 lain-Barre syndrome that selectively affects motor nerves, despite reports that GD1a is present in hu

90 s alter either motor neuron specification or motor nerve development, and highlight the importance of

91 CNS-born glia that critically contributes to motor nerve development.

92 ion-channel dysfunction (ATP7A and TRPV4) in motor-nerve disease.

93 key factor in the selective vulnerability of motor nerves due to their extraordinary length and evide

94 ATP is also released from sensory-motor nerves during antidromic reflex activity, to produ

95 Recordings of extraocular and limb motor nerves during spontaneous "fictive" swimming in is

96 e related to enhanced nociception, edema, or motor nerve dysfunction.

97 n extra- or intracellular action at the frog motor nerve ending.

98 patches were placed within 10 microns of the motor nerve ending.

99 denosine inhibits ACh release from mammalian motor nerve endings by reducing Ca(2+) calcium entry thr

100 ium channels or, as is the case at amphibian motor nerve endings, by an effect downstream of Ca(2+) e

101 nts by A(1) adenosine receptors at mammalian motor nerve endings.

102 with decreases in calcium currents at mouse motor nerve endings.

103 tes downstream of calcium entry at amphibian motor nerve endings.

104 facilitatory nicotinic ACh receptors on the motor nerve endings.

105 ial glia and Schwann cells was necessary for motor nerve ensheathment by both cell types.

106 The effects of temperature on parameters of motor nerve excitability were investigated in 10 healthy

107 inical and functional assessment, along with motor-nerve excitability studies, were undertaken in 10

108 hemical studies demonstrate that sensory and motor nerves express similar quantities of GD1a and GM1

109 abrupt onset characterized pathologically by motor nerve fiber degeneration of variable severity and

110 varicosites along excitatory and inhibitory motor nerve fibres increased and decreased respectively,

111 igin of perineurial cells and their roles in motor nerve formation are poorly understood.

112 ucture, the perineurium, which ensheaths the motor nerve, forming a flexible, protective barrier.

113 as performed of the intramuscular courses of motor nerves from the deep orbit to the anterior extents

114 The lack of an H reflex despite normal motor nerve function in the hindlimbs of these mutants s

115 growth factor expression between sensory and motor nerve, grafts of cutaneous nerve or ventral root w

116 ption factor foxc1a is dispensable for trunk motor nerve guidance but is required to guide spinal ner

117 with electrical stimulation of a peripheral motor nerve has been used to produce a lasting modulatio

118 ether this deficit of immunoreactive sensory-motor nerves has a functional counterpart in vivo.

119 red for pathfinding and targeting of the SNb motor nerve in Drosophila.

120 or nerves, the phrenic nerve, and the dorsal motor nerve in fore- and hindlimbs.

121 te extraocular muscles (EOMs) and associated motor nerves in Duane retraction syndrome (DRS) linked t

122 Conversely, motor nerves in Mmp1 and Mmp2 single mutants and Mmp1 Mm

123 The basis of preferential motor nerve injury in this disease is not clear, however

124 brates are intrinsically 'pre-patterned' for motor nerve innervation.

125 parent LR innervation by the inferior rectus motor nerve is an overlapping feature of Duane retractio

126 s indicate that selective binding of mAbs to motor nerves is not due to differences in antibody affin

127 e formation of the Drosophila intersegmental motor nerve (ISN).

128 urotrophic factors (NFs) to the cut stump of motor nerves of neonatal rats confers neuroprotection fr

129 Furthermore, myelination was disrupted in motor nerves of zebrafish lacking alphaII spectrin.

130 y sustained periods of endurance exercise or motor nerve pacing, as assessed by expression in trans g

131 ractice pathway for the evaluation of ocular motor nerve palsies has been developed for isolated sixt

132 of older patients with isolated acute ocular motor nerve palsies regardless of whether vascular risk

133 eries of patients with acute isolated ocular motor nerve palsies, a substantial proportion of patient

134 , primary motoneurons pioneer the peripheral motor nerve pathways, and the axons of secondary motoneu

135 Motor nerves play the critical role of shunting informat

136 1-20 Hz) caused Ca(2+) transients in enteric motor nerve processes and then in PDGFRalpha(+) cells sh

137 ptors were blocked, a single stimulus to the motor nerve produced channel openings in the detector pa

138 ression of IGF-1 in skeletal muscle enhances motor nerve regeneration after a nerve crush injury.

139 ity, and when absent, destabilization of the motor nerves results in muscle regeneration and in atrop

140 Although the most distal processes of the motor nerves retract following the degeneration of larva

141 We monitored respiratory-related motor nerve rhythm in neonatal rodent slice preparations

142 ecorded early in development are the cranial motor nerve roots that exit the hindbrain, the motor neu

143 Intracellular recordings from the motor nerve showed both fast and slow voltage- and activ

144 nvestigate the possibility that deefferented motor nerves sprout to new muscle targets.

145 muscle subjected to continuous low frequency motor nerve stimulation (3 V, 10 Hz).

146 ted how elevated quantal release produced by motor nerve stimulation affects the size of the quanta.

147 cteristics are dependent on the frequency of motor nerve stimulation and are thought to be controlled

148 Prolonged trains of cholinergic motor nerve stimulation failed to activate slow waves in

149 potentials (EJPs) evoked in these muscles by motor nerve stimulation revealed a large, apparently sto

150 orced expression of activated calcineurin or motor nerve stimulation up-regulates a MEF2-dependent re

151 mean amplitude) contractions in response to motor nerve stimulation with unchanging spike bursts con

152 e adaptive response of skeletal myofibers to motor nerve stimulation.

153 o, at specific choice points along the major motor nerves, subsets of motor axons defasciculate and t

154 ally, we found that PUM2 is regulated by the motor nerve suggesting a trans-synaptic mechanism for lo

155 esponse to agrin, which is secreted from the motor nerve terminal and induces the clustering of acety

156 from entering the synaptic cleft between the motor nerve terminal and the muscle fibre.

157 e robust influence of rearing temperature on motor nerve terminal arborization.

158 sher syndrome with particular respect to the motor nerve terminal as a potential site of injury, and

159 increased neurotransmitter release from the motor nerve terminal at low [Ca2+] in the presence of th

160 The presynaptic motor nerve terminal at the neuromuscular junction (NMJ)

161 ated with the loss of synaptic vesicles from motor nerve terminal boutons, a decline in immunoreactiv

162 s proposed that tirilazad suppresses delayed motor nerve terminal Ca2+ conductances secondary to its

163 tirilazad are involved in the suppression of motor nerve terminal excitability.

164 Q1b antibodies have been shown to damage the motor nerve terminal in vitro by a complement-mediated m

165 We considered that rapid AGAb uptake at the motor nerve terminal membrane might attenuate complement

166 nium response indicative of a suppression of motor nerve terminal repetitive discharge.

167 mission in this study reveals defects in the motor nerve terminal that may compensate for the muscle

168 What causes a motor nerve terminal to degenerate remains unknown.

169 The data show that it is not necessary for a motor nerve terminal to occupy most of an endplate, or t

170 , which are the glia cells juxtaposed to the motor nerve terminal, actively participate in multiple a

171 The tripartite motor synapse consisting of motor nerve terminal, terminal Schwann cells (tSCs) and

172 Using the frog motor nerve terminal, which contains especially large ac

173 ecisely mirrors the branching pattern of the motor nerve terminal.

174 e (DHP)-sensitive L-type Ca2+ current at the motor nerve terminal.

175 GRP) is found in dense-cored vesicles in the motor nerve terminal.

176 scular junction, and structure of the larval motor nerve terminal.

177 nding to cannabinoid type 1 receptors on the motor nerve terminal.

178 malian central nervous system and Drosophila motor nerve terminal.

179 Agrin released from motor nerve terminals activates a muscle-specific recept

180 f P/Q-type voltage-gated calcium channels at motor nerve terminals and consequent reduction in acetyl

181 (ICC-IM) are closely associated with enteric motor nerve terminals and electrically coupled to smooth

182 ivity and functional bridges between enteric motor nerve terminals and gastrointestinal smooth muscle

183 IC-IM were intimately associated with motor nerve terminals and nerve varicosities formed syna

184 upted in cultured myotubes in the absence of motor nerve terminals and Schwann cells, agrin-induced A

185 get muscle fibers in the maintenance of frog motor nerve terminals at synaptic sites.

186 es were able to bind and disrupt presynaptic motor nerve terminals at the neuromuscular junction (NMJ

187 stable beta-catenin specifically in muscles, motor nerve terminals became extensively defasciculated

188 dependent repetitive discharge of the soleus motor nerve terminals due to an exaggeration of the nerv

189 ndria sequester much of the Ca2+ that enters motor nerve terminals during repetitive stimulation at f

190 xo- and endocytosis at 37 degrees C in mouse motor nerve terminals expressing synaptopHluorin (spH),

191 -100 Hz) were recorded from mouse and lizard motor nerve terminals filled with a low-affinity fluores

192 asure the time course of endocytosis in frog motor nerve terminals following tetanic nerve stimulatio

193 Motor nerve terminals from amyotrophic lateral sclerosis

194 e show P2X7 receptor subunits on presynaptic motor nerve terminals from birth, but no evidence for P2

195 (miniature endplate potentials (MEPPs)) from motor nerve terminals has been examined in skeletal musc

196 elationship of exocytosis and endocytosis in motor nerve terminals has been explored, with varied res

197 CaMKII activation increases PI3K activity in motor nerve terminals in a DFak-dependent manner, even i

198 d induced ultrastructural alterations of the motor nerve terminals in mice in vivo.

199 molecules are thought to induce sprouting of motor nerve terminals in response to paralysis.

200 c function was investigated at K+-stimulated motor nerve terminals in snake costocutaneous nerve musc

201 y-induced anterograde degeneration of soleus motor nerve terminals in the cat.

202 Motor nerve terminals in this genotype contained more sy

203 potentials (50 Hz for 10-50 s) delivered to motor nerve terminals innervating external intercostal m

204 Motor nerve terminals innervating fibres in the transver

205 In addition, synaptic bouton structure at motor nerve terminals is altered.

206 Neurotransmitter release from frog motor nerve terminals is strongly modulated by change in

207 that the cues that confer stability to frog motor nerve terminals likely reside external to muscle f

208 Furthermore, motor nerve terminals loaded with the vital dye FM1-43 i

209 )styryl) pyridinium dibromide] stained mouse motor nerve terminals obtained from wild-type (WT) and s

210 Degeneration of motor nerve terminals occurs in amyotrophic lateral scle

211 alcium and altered morphology are present in motor nerve terminals of amyotrophic lateral sclerosis p

212 timulus-dependent changes of cytosolic Ca at motor nerve terminals of csp mutant Drosophila.

213 major component of the clearance occurred at motor nerve terminals of neuromuscular junctions, from w

214 xpressed in neurons, such as motoneurons and motor nerve terminals of the neuromuscular junction (NMJ

215 spinal cord, especially in motor neurons and motor nerve terminals of the neuromuscular junction (NMJ

216 cle protein SV2A is selectively localized in motor nerve terminals on slow (type I and small type IIA

217 t sizes ranged in distribution from 3 to 111 motor nerve terminals per unit.

218 Repeated observation of motor nerve terminals showed that nerve terminals were w

219 ic staining and destaining of FM1-43 in frog motor nerve terminals suggested that staurosporine might

220 e changes in the evoked ACh release from rat motor nerve terminals that are consistent with the exist

221 ynaptic vesicles in top views of living frog motor nerve terminals that had been prestained with the

222 used IgG antibodies to presynaptic VDCCs at motor nerve terminals that underlie muscle weakness in t

223 trains of action potentials were measured in motor nerve terminals using a rapidly scanning confocal

224 he reserve pool of synaptic vesicles in frog motor nerve terminals using fluorescence microscopy, ele

225 NT/B entry into PC12 cells and rat diaphragm motor nerve terminals was activity dependent and can be

226 urally intact up to 7 weeks after injury and motor nerve terminals were robustly preserved even in ol

227 Motor nerve terminals were transiently associated with b

228 Monoethylcholine (MECH) enters motor nerve terminals where it is made into acetylmonoet

229 c specializations only partially occupied by motor nerve terminals, and muscle fiber atrophy and dege

230 nt Protein transgenically expressed in mouse motor nerve terminals, and report that Ca(2+) influx eli

231 hat a P2X7-like receptor is present at mouse motor nerve terminals, and that their activation promote

232 hological defects were largely restricted to motor nerve terminals, as the ultrastructure of motoneur

233 n fluorescent protein in neurones, axons and motor nerve terminals, including the 'brainbow' mouse tr

234 s to an increased frequency of SV2A-positive motor nerve terminals, indicating a fiber type-specific

235 effect on the synaptic physiology of larval motor nerve terminals, it fully suppresses the decrease

236 J) is a tripartite synapse that is formed by motor nerve terminals, postjunctional muscle membranes,

237 At motor nerve terminals, SERCA inhibition retards calcium

238 or endplates does not correlate with loss of motor nerve terminals, signifying that one can occur in

239 neurotransmitter release at csp null mutant motor nerve terminals, suggesting widely overlapping fun

240 nd actin dynamics on vesicle cycling in frog motor nerve terminals, using fluorescence and electron m

241 oped progressive adult-onset degeneration of motor nerve terminals, whereas GFP-Syb2 and Ub(G76V)-GFP

242 inal sprouting, and poor arborization of the motor nerve terminals, whereas postsynaptic acetylcholin

243 amate application to activate PI3K in larval motor nerve terminals, whereas transgene-induced CaMKII

244 : 100 microM), triggers vesicle release from motor nerve terminals, which is blocked by P2X7RS-specif

245 , Phr1 functions cell-autonomously to sculpt motor nerve terminals.

246 re the mobility of synaptic vesicles in frog motor nerve terminals.

247 ocalization of BoNT/C1 ad with diaphragmatic motor nerve terminals.

248 e required for neurotransmitter release from motor nerve terminals.

249 that regulate acetylcholine (ACh) release at motor nerve terminals.

250 aled that the P2X(7) receptor was present in motor nerve terminals.

251 rized two vesicle recycling pathways in frog motor nerve terminals.

252 R101), to view endocytic events within snake motor nerve terminals.

253 duced by physiological stimulation of lizard motor nerve terminals.

254 ys) on the excitability of normal cat soleus motor nerve terminals.

255 f multiple subtypes of VSCCs at newly formed motor nerve terminals.

256 f extracellularly recorded currents at mouse motor nerve terminals.

257 f the exocytic machinery component SNAP25 in motor nerve terminals.

258 has been used to measure quantal turnover in motor nerve terminals.

259 b2) that develop progressive degeneration of motor nerve terminals.

260 neurotransmitter release at human peripheral motor nerve terminals.

261 ent light (NF-L) protein in distal axons and motor nerve terminals.

262 for the differentiation and stabilization of motor nerve terminals.

263 A-dependent activation of PI3K at Drosophila motor nerve terminals.

264 relatives, SV2B and SV2C, are present in all motor nerve terminals.

265 on neurotransmitter release from sensory and motor nerve terminals.

266 ts of organizers act sequentially to pattern motor nerve terminals: FGFs, beta2 laminins, and collage

267 recruitment was greater in the contralateral motor nerve than in the ipsilateral nerve.

268 he human tongue is supplied more richly with motor nerves than are those of living apes and propose t

269 As a result, spinal motor nerves that were modulated by the previously intac

270 al growth in the VII(th) and XII(th) cranial motor nerves, the phrenic nerve, and the dorsal motor ne

271 yos, the sharp inward turn taken by the ISNb motor nerve to approach its muscle targets.

272 SCPs migrate along the visceral motor nerve to the vicinity of the forming adrenal gland

273 try, which generates patterned discharges in motor nerves to appropriate muscles.

274 An action potential in a motor nerve triggers an action potential in a muscle cel

275 he lateral (LR) and medial rectus (MR) EOMs, motor nerve trunks bifurcated into approximately equal-s

276 ay arise from pathology affecting the distal motor nerve up to the level of the anterior horn cell.

277 x2 function, isthmic nuclei, the cerebellum, motor nerve V, and other derivatives of rhombomeres 1-3

278 The motor nerve was stimulated at 10 Hz in preparations in w

279 Orbital motor nerves were typically small, with the abducens ner

280 e seen on development of cranial and primary motor nerves, which were severely stunted as late as sta

281 Homarus americanus by stimulating a cardiac motor nerve with rhythmic bursts of action potentials an

282 onstrated diffuse involvement of sensory and motor nerves, with loss of myelin in the posterior colum

283 ial stages of synapse formation, sensory and motor nerves withdrew and degenerated.