ライフサイエンスコーパス: motor nerve

1 age-matched controls (~15 m/s difference in motor nerves).

2 oduce identical phenotypes affecting the SNa motor nerve.

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

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

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

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

7 on and resulted in conduction alterations in motor nerves.

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

9 entials evoked by stimulating postganglionic motor nerves.

10 lectrodes were placed bilaterally on the SNB motor nerves.

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

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

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

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

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

16 mice studies of large myelinated sensory and motor nerves.

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

18 or forming and maintaining functional spinal motor nerves.

19 st unchanged even after damage to downstream motor nerves.

20 by the interaction between muscle fibres and motor nerves.

21 ed their 'fictive' patterns from respiratory motor nerves.

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

23 expression was also able to generate ectopic motor nerves.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 possibly substance P) released from sensory-motor nerves and vasoconstriction caused by noradrenalin

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

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

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

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

49 Consistent segregation of intramuscular motor nerve arborization suggests functionally distinct

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

51 As such, spinal motor nerves are expected to be susceptible to oxidative

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

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

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

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

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

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

58 ed to stimulate major dilatation via sensory-motor nerves but induced sympathetic beta(1) -adrenocept

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

60 f the motor signal and a single spike in the motor nerve can be associated with ~50% inhibition of gl

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

62 ssive neurodegenerative disease that affects motor nerve cells in the brain and the spinal cord.

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

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

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

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

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

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

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

70 Motor nerve conduction velocities of the fastest fibers

71 Motor nerve conduction velocities showed normal values (

72 Moreover, motor nerve conduction velocities were increased in trea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 Motor nerve conduction velocity was moderately reduced i

88 Sciatic motor nerve conduction velocity, hindlimb digital sensor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 facilitatory nicotinic ACh receptors on the motor nerve endings.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 Perivascular sensory-motor nerves have been shown to cause vasodilatation in

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

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

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

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

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

134 anisms active at the end target muscle after motor nerve injury reveals new therapeutic targets that

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

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

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

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

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

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

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

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

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

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

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

146 Motor nerves play the critical role of shunting informat

147 1-20 Hz) caused Ca(2+) transients in enteric motor nerve processes and then in PDGFRalpha(+) cells sh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 MJ has a very brief AP waveform and that the motor nerve terminal contains three distinct electrical

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

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

177 s in the AP waveform along the length of the motor nerve terminal may explain the proximal-distal gra

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

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

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

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

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

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

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

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

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

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

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

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

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

191 malian central nervous system and Drosophila motor nerve terminal.

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

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

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

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

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

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

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

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

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

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

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

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

204 -100 Hz) were recorded from mouse and lizard motor nerve terminals filled with a low-affinity fluores

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

206 Motor nerve terminals from amyotrophic lateral sclerosis

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

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

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

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

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

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

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

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

215 Motor nerve terminals in this genotype contained more sy

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

217 Motor nerve terminals innervating fibres in the transver

218 bility of these toxins to target and bind to motor nerve terminals is a key factor determining their

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

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

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

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

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

224 Degeneration of motor nerve terminals occurs in amyotrophic lateral scle

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 Motor nerve terminals were transiently associated with b

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

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

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

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

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

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

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

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

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

251 At motor nerve terminals, SERCA inhibition retards calcium

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

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

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

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

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

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

258 : 100 microM), triggers vesicle release from motor nerve terminals, which is blocked by P2X7RS-specif

259 on neurotransmitter release from sensory and motor nerve terminals.

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

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

262 e required for neurotransmitter release from motor nerve terminals.

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

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

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

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

267 duced by physiological stimulation of lizard motor nerve terminals.

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

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

270 f extracellularly recorded currents at mouse motor nerve terminals.

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

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

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

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

275 neurotransmitter release at human peripheral motor nerve terminals.

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

277 for the differentiation and stabilization of motor nerve terminals.

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

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

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

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

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

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

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

285 Using trains of stimuli to motor nerves timed as a Poisson process and coherence an

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

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

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

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

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

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

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

293 Besides, NINMs can increase motor nerves velocity (ES = 1.82; 95% CI = 1.47 to 2.17)

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

295 Given that the facial nerve is a pure motor nerve, we presume that the afferent fibres respons

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

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

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

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

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