ライフサイエンスコーパス: motor neuron

1 crease in axonal reinnervation of the lumbar motor neurons.

2 , often fatal muscle weakness due to loss of motor neurons.

3 s following C9orf72 transgenic expression in motor neurons.

4 ressive axonal degeneration mainly affecting motor neurons.

5 sgenic restoration of Zfp106 specifically in motor neurons.

6 he potassium channel Kv2.1 at the surface of motor neurons.

7 s a progressive neurodegenerative disease of motor neurons.

8 of the human ataxin-3 protein is limited to motor neurons.

9 ts and induced pluripotent stem cell-derived motor neurons.

10 l sclerosis (ALS) leads to selective loss of motor neurons.

11 human induced pluripotent stem cell-derived motor neurons.

12 neurodegeneration of the corticospinal tract motor neurons.

13 ressed in posterior, but not anterior, vagus motor neurons.

14 e neuronal cell types: retinal, sensory, and motor neurons.

15 tissues impacted by a SMN deficiency beyond motor neurons.

16 contact them, including satellite cells and motor neurons.

17 eneration in the neuronal cell lines and rat motor neurons.

18 pes in multiple cellular contexts, including motor neurons.

19 provide recurrent inhibitory feedback to the motor neurons.

20 t in ALS mutant SOD1-expressing cortical and motor neurons.

21 ice due to infection and loss of spinal cord motor neurons.

22 the initial steep increase in firing rate in motor neurons.

23 he survival of distinct classes of embryonic motor neurons.

24 lloproteinase 9 and is selectively toxic for motor neurons.

25 rvate the human upper limb, of which 10% are motor neurons.

26 onal and synaptic plasticity on ventral horn motor neurons.

27 r disease characterized by the loss of lower motor neurons.

28 binger of dysfunction and aberrant firing of motor neurons.

29 e involving dying-back degeneration of upper motor neurons.

30 lass-specific effector genes in post-mitotic motor neurons.

31 imulates outgrowth of neurites from cultured motor neurons.

32 hic lateral sclerosis (ALS) and is toxic for motor neurons.

33 NAi suppressor screen identified survival of motor neuron 1 (SMN-1) as a downstream effector.

34 Homozygous loss of the gene survival of motor neuron 1 (SMN1) causes the selective degeneration

35 ed by deletions or mutations of the Survival Motor Neuron 1 (SMN1) gene coupled with predominant skip

36 caused by deletions or mutations of Survival Motor Neuron 1 (SMN1) gene.

37 cement of the mutated gene encoding survival motor neuron 1 (SMN1) in this disease.

38 ss and caused by mutations in SMN1 (Survival Motor Neuron 1).

39 ality, is caused by the loss of the survival motor neuron-1 (SMN1) gene, which leads to motor neuron

40 he splicing deficit of the SMN2 (survival of motor neuron 2) gene have been identified and these mole

41 n premotor interneurons (AVA) and downstream motor neurons (A-MNs) in the Caenorhabditis elegans esca

42 sed the same neurotransmitters as endogenous motor neurons-acetylcholine and a combination of adenosi

43 Our results indicate that motor neurons activate this bottom-up connection, and bl

44 itatory V3 neurons, and segmented excitatory motor neuron activity into sub-networks.

45 When motor neuron activity was recorded while the inhibitory

46 which precise premotor rhythms are tuned by motor neuron activity.SIGNIFICANCE STATEMENT Central pat

47 insights into the role of afferent input on motor neuron activity.SIGNIFICANCE STATEMENT Targeted mu

48 tion is surprisingly efficient in preventing motor neuron and cerebellar atrophy, as demonstrated in

49 preservation of myelinated white matter and motor neurons and an increase in axonal reinnervation of

50 can be rescued by expression of cacophony in motor neurons and by expression in two pairs of neurons

51 PPIA, MM218, given at symptom onset, rescued motor neurons and extended survival in the SOD1(G93A) mo

52 of the ALS-linked mutants of SOD1 in primary motor neurons and in a Danio rerio (zebrafish) model of

53 Circuits composed of both motor neurons and interneurons were established, but the

54 ve disorder that is characterized by loss of motor neurons and shows clinical, pathological, and gene

55 f polyglutamine-expanded AR causes damage to motor neurons and skeletal muscle cells.

56 ) causes the selective degeneration of lower motor neurons and subsequent atrophy of proximal skeleta

57 NCE STATEMENT The inadequate excitability of motor neurons and their output, the neuromuscular juncti

58 ential receptor subunit in a large subset of motor neurons (and all skeletal muscle, as shown in this

59 ts (the muscle fibers innervated by a single motor neuron) and manipulating patterns of activation of

60 inhibitor reduced neuroinflammation, rescued motor neurons, and extended survival in the SOD1(G93A) m

61 rom a set of proteins that are metastable in motor neurons, and thus prone to aggregation upon a dise

62 come essential for ChAT maintenance when the motor neurons are challenged by nerve crush.

63 In vertebrates, motor neurons are not commonly known to contribute to CP

64 cy pathways linking motor cortex with spinal motor neurons are selectively activated during one behav

65 KEY POINTS: Motor neurons are the output neurons of the central nerv

66 ified a defect in repetitive firing of lower motor neurons as a novel contributor to intensive care u

67 vity is enriched in corticospinal and spinal motor neurons as well as in oligodendrocytes in brain re

68 onset, improved motor function and preserved motor neurons as well as neuromuscular junctions from de

69 hagy gene Atg7 was specifically disrupted in motor neurons (Atg7 cKO).

70 ctional movements of mitochondria in primary motor neuron axons expressing wild type and mutant Hsp27

71 o showed that TBPH mutants displayed reduced motor neuron bursting and coordination during crawling a

72 c factors promote the survival of developing motor neurons but their combinatorial actions remain poo

73 cular atrophy (SMA) is caused by the loss of motor neurons, but astrocyte dysfunction also contribute

74 does not affect ChAT labeling in nonlesioned motor neurons, but it significantly increases the loss o

75 S exert an unknown gain-of-toxic function in motor neurons, but mechanisms underlying this effect rem

76 ration of the native interaction partners in motor neurons, but not when scores are generated from an

77 nterneurons that provided synaptic inputs to motor neurons, but the pharmacologic properties of inter

78 SMA is characterized by loss of motor neurons, but the underlying mechanism is largely u

79 rotective effect in SMA model mice and human motor neuron cell culture systems.

80 Autophagy inhibition did not prevent motor neuron cell death, but it reduced glial inflammati

81 However, in a motor neuron cell line, NSC34, E478G mutant of OPTN but

82 ng is closely associated with the molding of motor neuron character proposing the existence of a conc

83 t axon guidance choices within the GABAergic motor neuron circuit.

84 Recordings revealed that sensory and motor neurons comingle within laminae of the SC to suppo

85 roposing a paradigm for investigating spinal motor neuron contribution to skeletal joint mechanical f

86 These motor neurons control expiratory pressure and laryngeal

87 Reticulospinal neurons project to spinal motor neurons controlling hand muscles and extensively s

88 clude loss of lower (ventral horn) and upper motor neurons (corticospinal motor neurons in layer V),

89 uperoxide dismutase 1 (SOD1) protein between motor neurons could be detected in intact chimeric mice.

90 ion of RNA:DNA hybrid structures, leading to motor neuron death.

91 The number of motor neurons decreased substantially at 24 hours after

92 neuron (SMN) protein and is characterized by motor neuron degeneration and muscle atrophy.

93 warranted and may be an important driver for motor neuron degeneration in ALS.

94 astrocytes have been shown to contribute to motor neuron degeneration in amyotrophic lateral scleros

95 of the resulting founder (F0) mice developed motor neuron degeneration, others displayed phenotypes c

96 how that Zfp106 knockout mice develop severe motor neuron degeneration, which can be suppressed by tr

97 in and microtubule cytoskeletons, leading to motor neuron degeneration.

98 yotrophic lateral sclerosis (ALS) is a fatal motor neuron degenerative disease.

99 Using motor neurons derived from induced pluripotent stem cell

100 ient in supporting both WT and SMN-deficient motor neurons derived from male, female, and mixed-sex s

101 ed single-cell RNA sequencing to compare two motor neuron differentiation protocols: a standard proto

102 ntiation in vitro in response to inducers of motor neuron differentiation.

103 We use complete alpha-motor neuron discharge series to drive forward subject-s

104 electrical activity to decode accurate alpha-motor neuron discharges across five lumbosacral segments

105 measurements of progression in patients with motor neuron disease (MND), as tools for future clinical

106 FTD overlaps extensively with the motor neuron disease amyotrophic lateral sclerosis (ALS)

107 s1 gene has been linked to congenital lethal motor neuron disease and X-linked intellectual disabilit

108 inal muscular atrophy (SMA) is a progressive motor neuron disease causing loss of motor function and

109 erosis (ALS) is a heterogeneous degenerative motor neuron disease linked to numerous genetic mutation

110 l sclerosis (ALS) is a multifactorial lethal motor neuron disease with no known treatment.

111 , and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and on

112 FTLD-TDP (55 nine type A including one with motor neuron disease, 27 type B including 21 with motor

113 neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal l

114 the pathological role of mutant profilin1 in motor neuron disease, we generated transgenic lines of m

115 A), the most common lethal genetic childhood motor neuron disease.

116 eases including Alzheimer's, Parkinson's and motor neuron disease.

117 (ALS) is the most common adult degenerative motor neuron disease.

118 otor neuropathy and LMN variants of familial motor neuron disease.

119 We revealed that motor-neuron disease (MND)-linked RNA-binding proteins (

120 use of neurotrophic factors in degenerative motor neuron diseases such as amyotrophic lateral sclero

121 Konzo is an irreversible upper-motor neuron disorder affecting children dependent on bi

122 hly heterogeneous group of neurodegenerative motor neuron disorders characterized by spastic parapare

123 ry synaptic drive in shaping the function of motor neurons during development and the contribution of

124 factor (HGF), by tissues innervated by vagal motor neurons during fetal development reveal potential

125 or classes of spinal interneurons as well as motor neurons during spasms in a mouse model of chronic

126 on in proprioceptive synaptic drive leads to motor neuron dysfunction and motor behavior impairments.

127 g neurodegenerative disease characterized by motor neuron dysfunction and progressive weakening of th

128 ted with bulbar onset and dysfunction, upper motor neuron dysfunction, cognitive impairment, depressi

129 the burden of clinical and electromyographic motor neuron dysfunction.

130 nduce the specification of digit-innervating motor neurons, emphasizing the specialized status of dig

131 Binding of Isl1/Lhx3 to later motor neuron enhancers depends on the Ebf and Onecut TFs

132 aired-pulse intracortical inhibition, spinal motor neuron excitability (F-waves), index finger abduct

133 ons that have been associated with increased motor neuron excitability and decreased inhibition.

134 rotonin receptors on motor neurons increases motor neuron excitability, in part by enhancing subthres

135 ALS-affected motor neurons exhibit aberrant localization of a nuclear

136 Motor neurons exhibit the most profound loss, but the me

137 silencer ISS-N1, which controls survival of motor neuron exon 7 splicing.

138 hat at larval neuromuscular junctions (NMJ), motor neuron expression of wild-type human PFN1 increase

139 Dendritic projections of dye back-filled motor neurons extend throughout a ventral layer of the S

140 Recent evidence suggests that motor neuron extrinsic influences, such as those arising

141 ircuits where the functional significance of motor neuron feedback is still poorly understood.

142 ly responsible for the initial sharp rise in motor neuron firing rate.

143 transmission, we observed a decrease in the motor neuron firing that could be explained by the reduc

144 a crucial role in the recruitment of spinal motor neurons following spinal cord injury.

145 The study of the behavior of motor neurons following this surgery is needed for desig

146 oxide dismutase 1 (SOD1(G93A)), we show that motor neurons form large autophagosomes containing ubiqu

147 ite their different developmental histories, motor neurons from both protocols structurally, function

148 he cellular model with laser-captured spinal motor neurons from C9ORF72-ALS cases, we also demonstrat

149 However, motor neurons from neonatal mice lacking VIAAT in Rensha

150 ting their physiological muscle targets with motor neurons from the same spinal segment whose axons w

151 indicates a possible approach for improving motor neuron growth and survival in this disease.

152 but the brain center that coordinates these motor neurons has not been identified.

153 ptor complexes in distinct subsets of lumbar motor neurons: HGF supports hindlimb motor neurons throu

154 (anti-human vWF, CD45, GFAP, and Iba-1) and motor neuron histological analyses were performed in cer

155 rescence also in small cells neighboring the motor neurons, identified as mature gray matter oligoden

156 transcription factors critical for abducens motor neuron identity, including MAFB, or by heterozygou

157 NTF) administration promotes the survival of motor neurons in a wide range of models.

158 reased awareness of potential involvement of motor neurons in a wider range of CPGs, perhaps clarifyi

159 the specific vulnerability of corticospinal motor neurons in ALS.

160 ession in astrocytes is selectively toxic to motor neurons in co-culture, even when mutant protein is

161 e the human disease-with progressive loss of motor neurons in heterozygous animals.

162 horn) and upper motor neurons (corticospinal motor neurons in layer V), mutant profilin1 aggregation,

163 and in vivo dynamic voltage clamp of spinal motor neurons in septic rats were employed to explore po

164 and that genetically restoring cacophony in motor neurons in TBPH mutant animals was sufficient to r

165 acterized by degeneration of upper and lower motor neurons in the brain and spinal cord.

166 is characterised by the progressive loss of motor neurons in the brain and spinal cord.

167 ubcortical levels, in particular sensory and motor neurons in the brainstem and thalamus.

168 eroxide dismutase (SOD1) selectively affects motor neurons in the central nervous system (CNS), causi

169 When activating muscles, motor neurons in the spinal cord also activate Renshaw c

170 nd largely preserve serotonin innervation of motor neurons in the spinal cord.

171 uring voluntary contraction, firing rates of motor neurons increase steeply but then level out at mod

172 cologic activation of serotonin receptors on motor neurons increases motor neuron excitability, in pa

173 xon initiation is delayed in posterior vagus motor neurons independent of neuron birth time.

174 effect on the survival of intact or lesioned motor neurons, indicating that these adult CNTF receptor

175 ded estimation of ankle function purely from motor neuron information.

176 We compared the behavior of motor neurons innervating their physiological muscle tar

177 Motor neuron innervation determined the sites for AChR c

178 ll types highlight the role of the astrocyte-motor neuron interaction in the resulting metabolic phen

179 The results support the novel approach of motor neuron interfacing for prosthesis control and prov

180 Diversification of motor neurons into different classes, each characterized

181 e have previously shown that the assembly of motor neurons into nuclei depends on cadherin-mediated a

182 and of axonal outgrowth in mammalian primary motor neurons involved aberrant activation of the p38 MA

183 evation in NFL levels in patients with upper motor neuron involvement and FTD might reflect the corti

184 All 6 exhibited severe lower motor neuron involvement in addition to cognitive change

185 that aberrant splicing of genes expressed in motor neurons is involved in SMA pathogenesis, but incre

186 itochondrial redox imbalance in mutant Hsp27 motor neurons is likely to cause low level of oxidative

187 cate that an inhibitory signal, activated by motor neurons, is required for proper CPG function.

188 hly viable, and standardized embryonic mouse motor neurons isolated by a unique FACS technique.

189 functionally, and transcriptionally resemble motor neurons isolated from embryos.

190 ) impair axonal transport of mitochondria in motor neurons isolated from SOD1 G93A transgenic mice an

191 which PKC isoforms in the sensory neuron or motor neuron L7 are required to sustain each form of LTF

192 Dysfunction and death of motor neurons leads to progressive paralysis in amyotrop

193 the cytotoxicity of SOD1(G93A) expressed in motor neuron-like cells.

194 n and neurite length of WT and SMN-deficient motor-neuron-like cells in cell culture.

195 Lower motor neuron (LMN) syndromes typically present with musc

196 erative disease characterized by progressive motor neuron loss and caused by mutations in SMN1 (Survi

197 ical levels and have adult onset progressive motor neuron loss and denervation of neuromuscular junct

198 SMA is characterized by alpha-lower motor neuron loss and muscle atrophy, however, there is

199 ysis and premature death (type I) to limited motor neuron loss and normal life expectancy (type IV).

200 egenerative disease that is characterized by motor neuron loss and that leads to paralysis and death

201 increased miR-146a was sufficient to induce motor neuron loss in vitro, whereas miR-146a inhibition

202 l motor neuron-1 (SMN1) gene, which leads to motor neuron loss, muscle atrophy, respiratory distress,

203 ession did not improve astrocyte function or motor neuron loss.

204 a inhibition prevented SMA astrocyte-induced motor neuron loss.

205 those arising from astrocytes, contribute to motor neuron malfunction and loss.

206 Similar studies on postnatal motor neurons may provide a conceptual framework for the

207 Motor neuron (MN) diseases are progressive disorders res

208 scular junction (NMJ) dysfunction and spinal motor neuron (MN) loss.

209 enes that contribute to the specification of motor neuron (MN) subtype identity.

210 ys that integrate and regulate the output to motor neurons (MN); ultimately these drive contraction o

211 circRNAs expressed in in vitro-derived mouse motor neurons (MNs) and determined that the production o

212 pendent currents that activate strongly when motor neurons (MNs) are first recruited.

213 aenorhabditis elegans possesses 19 GABAergic motor neurons (MNs) called D MNs, which are divided into

214 muscular junction (NMJ) precedes the loss of motor neurons (MNs) in amyotrophic lateral sclerosis (AL

215 ALS) is a neurodegenerative disease in which motor neurons (MNs) in the brain and spinal cord are sel

216 generative disorder due to selective loss of motor neurons (MNs).

217 isorder characterized by loss of spinal cord motor neurons, muscle atrophy and infantile death or sev

218 The data suggest that, although neither motor neuron nor muscle CNTF receptors play a significan

219 ent of changes in SMN levels or increases in motor neuron numbers they nevertheless have a significan

220 Although phrenic motor neuron numbers were decreased in end-stage SOD1(G9

221 on TDP-43 positive cytoplasmic inclusions in motor neurons of ALS patients.

222 Repletion of this isoform of Agrin in the motor neurons of SMA model mice increases muscle fiber s

223 hyme of the respiratory tract and in phrenic motor neurons of the central nervous system led us to ad

224 ple, we predict that, within the class of DD motor neurons, only three (DD04, DD05, or DD06) should a

225 expression were increased in spared phrenic motor neurons (p < 0.05), consistent with increased Q-pa

226 sing ADL neurons and their post-synaptic SMB motor neuron partners via increased expression of the od

227 sent in 13 of 14 myelopathy episodes whereas Motor Neuron pattern was observed in 1 of 14 MRIs.

228 th or without contrast enhancement; and (2) "Motor Neuron" pattern: a symmetric involvement of the an

229 ntly smaller for the surgically reinnervated motor neuron pool with respect to the corresponding phys

230 h the dynamic binding behavior of TFs during motor neuron programming from features associated with c

231 Thus, motor neuron programming is the product of two initially

232 the uniquely efficient Ngn2, Isl1, and Lhx3 motor neuron programming pathway.

233 They were contained within a cluster of motor neurons projecting through the same nerve to inner

234 cause inactivation of Rdl and Galphao in the motor neurons reduced the larval body size.

235 Graft-derived excitatory and inhibitory motor neurons released the same neurotransmitters as end

236 Cacophony expression in motor neurons rescued mEPP frequency but not mEPP amplit

237 at positions where expiratory and laryngeal motor neurons reside.

238 Further, deletion of Hoxa5 in motor neurons resulted in abnormal diaphragm innervation

239 aping the excitability and synaptic input to motor neurons.SIGNIFICANCE STATEMENT We here provide a d

240 Low NFL levels in patients with lower motor neuron signs might be a prognostic indicator of mi

241 iatric changes, movement disorders and upper motor neuron signs.

242 y loss-of-function mutations in the survival motor neuron (SMN) 1 gene which encodes the SMN protein.

243 ine methyltransferase 5 (PRMT5) and survival motor neuron (SMN) complexes.

244 , mechanisms governing stability of survival motor neuron (SMN) isoforms are poorly understood.

245 SMA) is caused by the low levels of survival motor neuron (SMN) protein and is characterized by motor

246 alogous gene to SMN1, restoring the survival motor neuron (SMN) protein level in mouse models of SMA.

247 hy (SMA) is caused by diminished Survival of Motor Neuron (SMN) protein, leading to neuromuscular jun

248 ction of the ubiquitously expressed survival motor neuron (SMN) protein, owing to loss of the SMN1 ge

249 iency of the ubiquitously expressed Survival Motor Neuron (SMN) protein.

250 aused by insufficient expression of survival motor neuron (SMN) protein.

251 ed by insufficient levels of the Survival of Motor Neuron (SMN) protein.

252 isorder caused by low levels of the Survival Motor Neuron (SMN) protein.

253 SMA is caused by low levels of the survival motor neuron (SMN) protein.

254 caused by reduced expression of survival of motor neuron (SMN), a protein expressed in humans by two

255 The SMN1 protein product, survival of motor neuron (SMN), is ubiquitously expressed and is a k

256 sekeeping protein, which makes the primarily motor neuron-specific phenotype rather unexpected.

257 tations underlying ocular CCDDs alter either motor neuron specification or motor nerve development, a

258 hat converges separately onto the same final motor neuron state as the standard path.

259 The establishment of spinal motor neuron subclass diversity is achieved through deve

260 ng class-specific effector genes in specific motor neuron subsets via discrete cis-regulatory element

261 r how the specification of digit-innervating motor neuron subtypes parallels the elaboration of digit

262 ial mCherry did not transfer to G85R SOD1YFP motor neurons, suggesting that neither RNA nor organelle

263 y precedes dendritic arborization of primary motor neurons, suggesting that the structured neuropil c

264 The tight coupling with motor neurons suggests that Renshaw cells have an integr

265 played by endogenous CNTF receptors in adult motor neuron survival and ChAT maintenance, independent

266 ved behavioral disease outcomes and enhanced motor neuron survival, mainly in high-cell-dose mice.

267 lock in glutamate processing that may impact motor neuron survival.

268 ered met abolic pathways and their impact on motor neuron survival.

269 itability and a normal number of cholinergic motor neuron synapses, indicating a compensatory mechani

270 o39Leu and Arg140Gly mutant Hsp27 expressing motor neurons than in wild type Hsp27 neurons, although

271 m of SMN to regulate HoxA5 levels in phrenic motor neurons that control respiration.

272 nner in which premotor interneurons activate motor neurons that in turn drive muscles.

273 atched by distinct mechanisms for specifying motor neurons that innervate digit muscles.

274 calization and breathing overlap and rely on motor neurons that innervate laryngeal and expiratory mu

275 ses in the context of C.elegans ventral cord motor neurons that share common traits that are directly

276 thus positioning-in a population of cranial motor neurons, the facial branchiomotor neurons (FBMNs).

277 e in the maintenance of ChAT in intact adult motor neurons, the receptors become essential for ChAT m

278 lumbar motor neurons: HGF supports hindlimb motor neurons through c-Met; CNTF supports subsets of ax

279 hrough c-Met; CNTF supports subsets of axial motor neurons through CNTFRalpha; and Artemin acts as th

280 val factor for parasympathetic preganglionic motor neurons through GFRalpha3/Syndecan-3 activation.

281 cending neurons, which drive the jump muscle motor neuron to trigger an escape take off.

282 ibe here a molecular mechanism necessary for motor neurons to acquire subclass-specific traits in the

283 e graded expression of plateau potentials in motor neurons to generate spasms, and inhibitory interne

284 Agrin is utilized by motor neurons to stimulate the LRP4-MuSK receptor in mus

285 the motor nucleus (the putative location of motor neuron-to-interneuron connections).

286 The vagus motor neuron topographic map is therefore determined by

287 ismutase 1 (SOD1), which are associated with motor neuron toxicity in an inherited form of amyotrophi

288 minal selectors of other sensory, inter-, or motor neuron types now enables ectopically expressed CHE

289 nerative signaling is not neuroprotective in motor neurons undergoing C9orf72 toxicity.

290 d in trans within satellite cells and within motor neurons via the neuromuscular junction.

291 ork for studying the control and behavior of motor neurons when changing their target innervated musc

292 We focus on the vagus motor neurons, which are topographically arranged in bot

293 receptor 1 (EphB1) is upregulated in injured motor neurons, which in turn can activate astrocytes thr

294 s and for cholinergic function of sublateral motor neurons, which separately innervate the four body

295 of adult chimeric progeny were examined for motor neurons with cytosolic double fluorescence.

296 c input and could be voluntary controlled as motor neurons with natural innervation.

297 The objective was to assess whether motor neurons with nonphysiological innervation receive

298 Silencing motor neurons with the intracellular sodium channel bloc

299 ement, require an unexpectedly low number of motor neurons, with a large convergence of afferent inpu

300 ivity feeds back to maintain integrity among motor neurons within a nucleus.