ライフサイエンスコーパス: nerve cell

1 en by the leading edge, or growth cone, of a nerve cell.

2 laces Mg2+ from its binding sites within the nerve cell.

3 cone, are needed to guide the extension of a nerve cell.

4 port in metabolism and signal propagation in nerve cells.

5 as a decrease in fluorescence of dye-treated nerve cells.

6 ronment, including endothelial, stromal, and nerve cells.

7 s cannot be caused by sudden loss or gain of nerve cells.

8 ion of p21Cip1 and p27Kip1 in tangle-bearing nerve cells.

9 loped optic tectum and a severe reduction in nerve cells.

10 iquitous protein kinase in the physiology of nerve cells.

11 where they concentrated around tau-positive nerve cells.

12 the action of botulinum neurotoxin (BoNT) on nerve cells.

13 xicity involves its ability to actually kill nerve cells.

14 adult mammalian brain that can generate new nerve cells.

15 ymmetric sites of cell-cell adhesion between nerve cells.

16 tional control in local protein synthesis in nerve cells.

17 ll division, and signal transduction between nerve cells.

18 ose uptake, apoptosis and cell death in PC12 nerve cells.

19 ia the nose and then spread to its preferred nerve cells.

20 cific molecular activities within identified nerve cells.

21 differentiation and apoptosis in muscle and nerve cells.

22 an important role in the differentiation of nerve cells.

23 r the translation of the connexin-32 mRNA in nerve cells.

24 ansgene included ciliary body (CB) and optic nerve cells.

25 chondrial damage and induce demyelination of nerve cells.

26 laboration of behaviors that depend on these nerve cells.

27 s gliosis and clustering of microglia around nerve cells.

28 red for reactivation of HSV1 from latency in nerve cells.

29 rgic and GABAergic postsynaptic membranes in nerve cells.

30 to control through physiological activity in nerve cells.

31 erlying beta-amyloid-induced degeneration of nerve cells.

32 +)- and PKC-independent Cl- current in these nerve cells.

33 to require temporally structured activity of nerve cells.

34 the (8R)-lipoxygenase pathway within intact nerve cells.

35 r determinants on the surfaces of vertebrate nerve cells.

36 odies comprise rather simple arrangements of nerve cells.

37 troduction have not been tested in human GAN nerve cells.

38 ther, as a result of overactivity of certain nerve cells.

39 istic basis for long-term plastic changes in nerve cells.

40 istribution of cytosolic proteins in growing nerve cells.

41 wild-type sodium channels and in hippocampal nerve cells.

42 etermination of Abeta peptide aggregation on nerve cells.

43 hereby modify the excitability of muscle and nerve cells.

44 hat is usually associated with PV-containing nerve cells.

45 t, predominates and is detected in forebrain nerve cells.

46 CNS with little known about its function in nerve cells.

47 orylation, compared with HT22 non-neoplastic nerve cells.

48 ed the subtype diversity of in vitro derived nerve cells.

49 ubtype diversification of the two classes of nerve cells.

50 by tetanus toxin for the initial entry into nerve cells.

51 is and efflux of excitatory amino acids from nerve cells.

52 by the presence of filamentous inclusions in nerve cells.

53 In nerve cells, a select group of RNAs has been localized t

54 d the following cascade of events leading to nerve cell activity.

55 When one nerve cell acts on another, its postsynaptic effect can

56 d expression of doublecortin, polysialylated nerve cell adhesion molecule, neurogenic differentiation

57 proteins originally shown to be important in nerve cell adhesion, axon migration, and proper central

58 Nerve cells adjust their electrical excitability and the

59 o ways, by decreasing the capacitance of the nerve cell and by increasing its membrane resistance, bu

60 jor post-translational regulatory process in nerve cell and synapse function, but the published evide

61 In the developing nervous system, nerve cells and axons respond to various attractive and

62 of the CNS that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons, and

63 rons that formed synaptic contacts with host nerve cells and expressed and released glial cell line-d

64 y focused on mechanisms of hormone action on nerve cells and how these effects translate into the dis

65 op receptors in the postsynaptic terminal of nerve cells and potentiate or inhibit their function.

66 tain BCL-2 and/or SOD-1 synthesis in damaged nerve cells and thereby reduce apoptosis.

67 ced possibilities for organ transplantation, nerve cells and tissue healing, and other health benefit

68 consistent with a single origin of the gut, nerve cells, and muscle cells in the stem lineage of eum

69 rizing phase of the action potential in most nerve cells, and Nav channel localization to the axon in

70 ectric activity of excitable tissues such as nerve cells, and play important roles in many diseases.

71 ogy enables the direct observation of single nerve cell apoptosis in experimental neurodegeneration,

72 -scanning ophthalmoscopy to visualize single nerve cell apoptosis in vivo, which allows longitudinal

73 have been able to image changes occurring in nerve cell apoptosis over hours, days, and months and sh

74 tor heterocomplex in the midbrain raphe 5-HT nerve cells appear to have a trophic role in the central

75 s to the delivery of active BoNT/A LC to the nerve cell are discussed.

76 -recombinase fate mapping to determine which nerve cells are neural crest derived.

77 The mechanisms of PA-LTx in nerve cells are not well understood, but our previous fi

78 ous system, electrical signals passing along nerve cells are speeded by cells called oligodendrocytes

79 he I(f), I(h) and I(q) currents of heart and nerve cells, are activated by membrane hyperpolarization

80 wo new studies explore structural changes of nerve cells as a potential mechanism for memory formatio

81 rofilaments (NFs) are a major constituent of nerve cell axons that assemble from three subunit protei

82 C (HC) of tetanus toxin retains the specific nerve cell binding and transport properties of tetanus h

83 only on the surfaces of a limited subset of nerve cell bodies and processes.

84 osition and water content were determined in nerve cell bodies from CA1 areas of rat hippocampal slic

85 Thus, peripheral nerve cell bodies have greater blood flow than their axo

86 No loss of 5-HT nerve cell bodies in the rostral raphe nuclei was found,

87 tilled into the trachea retrogradely labeled nerve cell bodies located in the nodose and jugular gang

88 Although the location of the nerve cell bodies of spinal afferents is well known to r

89 expression of P2Y R immunoreactivity (ir) in nerve cell bodies was in the order of P2Y1 R > P2Y4 R >>

90 of the endoplasmic reticulum, vacuolation of nerve cell bodies, and abnormal reticular aggregates.

91 t ideal for localizing not only degenerating nerve cell bodies, but also distal dendrites, axons and

92 to 200 boutons distributed between 10 and 29 nerve cell bodies.

93 rograde propagation of Trk activation to the nerve cell bodies.

94 inals propagates through the axon toward the nerve cell body at an initial rate that exceeds that of

95 ulator that are co-localized within the same nerve cell body may distribute totally independently and

96 the adult, through intrinsic effects on the nerve cell body response to injury and via an androgen r

97 results in increased CGRP production in the nerve cell body.

98 ncer therapeutics cause death of postmitotic nerve cells both in vitro and in vivo.

99 he protection from oxidative stress afforded nerve cells by PKC activity requires the combined modula

100 ctive repair of lesions that are produced in nerve cells by reactive oxygen species generated as by-p

101 The tyrphostins protect nerve cells by three distinct mechanisms.

102 tinal smooth muscle strips devoid of enteric nerve cells can contract in response to stretch, suggest

103 concentrations of cyclic nucleotides within nerve cells can dramatically change their responses to a

104 Thus the behaviour of many nerve cells cannot be understood on the basis of microel

105 h a person's own immune system damages their nerve cells, causing muscle weakness, sometimes paralysi

106 spatiotemporally organized activity in local nerve cell circuits, not synchronous activity within and

107 brain and play a key role in the function of nerve cell circuits.

108 Optic nerve cells cocultured with activated microglia showed a

109 Nerve cells communicate with each other through two mech

110 When nerve cells communicate, vesicles from one neuron fuse w

111 s used to assay endopeptidase activity under nerve-cell conditions.

112 High densities of nerve cells containing corticotropin-releasing hormone (

113 ch to test whether neuropeptides secreted by nerve cells contribute to the spatial structure of micro

114 The nerve-cell cytoskeleton is essential for the regulation

115 tyrphostins against oxidative stress-induced nerve cell death (oxytosis).

116 nylyl cyclase (sGC) activity is required for nerve cell death caused by glutathione depletion.

117 ains, none captures the extensive pattern of nerve cell death found in the human disease.

118 idative stress is thought to be the cause of nerve cell death in many CNS pathologies, including isch

119 ses in glutathione (GSH) are associated with nerve cell death in Parkinson's disease.

120 Apoptotic nerve cell death is implicated in the pathogenesis of se

121 that the final pathway of glutamate induced nerve cell death is through a cGMP-modulated calcium cha

122 he etiology of the disease, the cause of the nerve cell death remains unknown.

123 esults are consistent with a role for p53 in nerve cell death that is distinct from its actions relat

124 Oxidative stress is implicated in the nerve cell death that occurs in a variety of neurologica

125 o protect against anoxia-induced excitotoxic nerve cell death.

126 and PKCdelta inhibitors block stress-induced nerve cell death.

127 why the loss of PKC activity contributes to nerve cell death.

128 e after reactive astrogliosis, a response to nerve cell death.

129 ) receptor agonists on DNA fragmentation and nerve cell death.

130 ever, about the cytotoxic pathway leading to nerve cell death.

131 hat in each of these disorders, the affected nerve cells degenerate as a result of these abnormal inc

132 Nerve cells depend on specific interactions with glial c

133 ession, also contribute to the generation of nerve cell diversity.

134 ta(1-42) oligomers play a role in triggering nerve cell dysfunction and death in Alzheimer's disease.

135 This was associated with extensive nerve cell dysfunction and severe paralysis by the age o

136 e detailed mechanisms of Mn neurotoxicity in nerve cells, especially in dopaminergic neurons are not

137 it is demonstrated that primary rat cortical nerve cells exposed to Abeta display a time-dependent in

138 protective of central nervous system-derived nerve cells exposed to oxidative stress were tested to s

139 ys upon prolonged exposure to Abeta in model nerve cells expressing nicotinic acetylcholine receptors

140 als show nerve regrowth, with axons from the nerve cells extending down towards the injury or re-rout

141 Nerve cells form elaborate, highly branched dendritic tr

142 operties, and possess the ability to protect nerve cells from death at the calcium overload condition

143 The role of this protein in nerve cell function is controversial, but here we provid

144 even before the photoreceptors are present, nerve cell function is essential for correct wiring of t

145 ent membrane assembly, as well as muscle and nerve cell function.

146 ium channels respond to excitatory inputs in nerve cells, generating spikes of depolarization at axon

147 not the result of loss of a particular 5-HT nerve cell group.

148 He showed that most nerve cells have a single axon and several dendrites; he

149 rve the movement of this protein in cultured nerve cells have been largely unsuccessful.

150 Recordings from single sensory nerve cells have yielded useful insights, but single neu

151 sfunction/death of vulnerable populations of nerve cells important in memory, higher cognitive proces

152 cles are essential for communication between nerve cells in a process mediated by neurotransmitters.

153 Many tau-positive nerve cells in brainstem and spinal cord were strongly i

154 se results indicate that amalgam is toxic to nerve cells in culture by releasing zinc.

155 The first tau aggregates form in a few nerve cells in discrete brain areas.

156 minergic neurons to replace the degenerating nerve cells in Parkinson disease looming, it is critical

157 metry and cocultured with neonatal rat optic nerve cells in separate but media-connected chambers.

158 system is the hormone leptin, which acts on nerve cells in the brain (and elsewhere) to regulate foo

159 l surface, enabling him to view the paths of nerve cells in the brain.

160 lieved to be associated with degeneration of nerve cells in the central nervous system of patients wi

161 nervous system neurons and certain groups of nerve cells in the CNS, cortical projection neurons are

162 lecules or CAMs), it is expressed on growing nerve cells in the developing nervous system of vertebra

163 ng between cortical interneurons and between nerve cells in the inferior olivary nucleus.

164 hich allow direct microscopic observation of nerve cells in the retina.

165 ed moderate to severe depletion of pigmented nerve cells in the substantia nigra in each case.

166 Protective effects of estrogen on nerve cells including retinal neurons have been describe

167 are not attributable to increased numbers of nerve cells, increased target size, or obvious changes i

168 ety of rodent models of neurodegeneration or nerve cell injury.

169 evaluated for use as a substrate to enhance nerve cell interactions in culture as a first step towar

170 Synapses join individual nerve cells into a functional network.

171 evelopmentally unrelated cell types, such as nerve cells into blood cells.

172 onnectivity depend on the diversification of nerve cells into functionally and molecularly distinct s

173 The primary function of the nerve cell is to process electrical signals.

174 abnormal filamentous inclusions within some nerve cells is a characteristic shared by Alzheimer's di

175 e to sulfhydryl oxidation in Abeta-resistant nerve cells is a compensatory response to the oxidative

176 Structural plasticity of nerve cells is a requirement for activity-dependent chan

177 factor (NGF), a classical trophic factor for nerve cells, is expressed in pancreatic vasculature whil

178 al production and lipid peroxidation in PC12 nerve cells, leading to increased 4-hydroxy-2-nonenal (H

179 immature cortical neurons and a hippocampal nerve cell line via an oxidative pathway associated with

180 immature cortical neurons and a hippocampal nerve cell line, HT22.

181 Using immature cortical neurons and a clonal nerve cell line, it is shown that a decrease in GSH trig

182 otentiate later transcriptional actions in a nerve cell line.

183 We show here that clonal nerve cell lines and primary cortical neurons that are r

184 glutamate-induced cell death in both clonal nerve cell lines and rat cortical neurons.

185 We previously demonstrated that nerve cell lines selected for resistance to amyloid beta

186 C-terminal helix deleted were affected with nerve cell loss in the hippocampus and proliferation of

187 Neuropathologically, progressive nerve cell loss, gliosis and coexistent neuronal and/or

188 e findings are indicative of active, ongoing nerve cell loss, suggesting that a time-limited insult t

189 of the human disease but show no significant nerve cell loss.

190 tau protein and neurodegeneration leading to nerve cell loss.

191 ent perforant tract, secondary to entorhinal nerve cell loss.

192 The cause of VH is now thought to be nerve-cell loss and Lewy-body pathology in the ventral-t

193 e microelectrode arrays to stimulate retinal nerve cells may provide a viable treatment for degenerat

194 onformational changes open a pore across the nerve cell membrane.

195 Nerve cell microcircuits are modified by excitatory and

196 endrites; he recognized the possibility that nerve cells might be functionally polarized and produced

197 the surface of neurons and is essential for nerve cell migration and the establishment of axonal pat

198 Using an experimental nerve cell model for oxidative stress and an expression

199 relation to phase singularities within local nerve cell networks.

200 neural excitability is essential for proper nerve cell, neural circuit, and nervous system function.

201 nced wiring, and forms of connectivity among nerve cells not found in any animal, challenging the vie

202 usion of 'cryptic' exons in messenger RNA in nerve cells, NOVA proteins are able to influence the abu

203 YP2J proteins were present at high levels in nerve cells of autonomic ganglia, epithelial cells, inte

204 ose pathological hallmark is the presence in nerve cells of proteinacious deposits, known as Lewy bod

205 phate and hyperphosphorylated tau coexist in nerve cells of the Alzheimer's disease brain at the earl

206 throughout development in the intestine and nerve cells of the head.

207 echnique should be capable of both switching nerve cells on and off within milliseconds in a non-inva

208 ration, 14 years) to receive a transplant of nerve cells or sham surgery; all were to be followed in

209 r Iq, were initially discovered in heart and nerve cells over 20 years ago.

210 cortical neurons, a predominantly GABAergic nerve cell population, and cerebral cortical astrocytes.

211 granule cells, a predominantly glutamatergic nerve cell population, has been investigated.

212 idbrain dopaminergic neurons (mesDA) are the nerve cells preferentially lost in the brains of Parkins

213 that memory formation requires the growth of nerve cell processes.

214 Tumor and nerve cell receptors provide such targets.

215 omatin immunoprecipitation (ChIP) of sciatic nerve cells revealed a Sox10 binding site upstream of an

216 l relevance of complex waves by showing that nerve cell spike rates are higher in presence of complex

217 within nanoscopic spaces outside and inside nerve cells, such as synaptic clefts or dendritic spines

218 stions on the gradient sensing properties of nerve cells, such as the sensitivity and robustness in t

219 Genetic studies focusing on nerve cells supplying the central complex from the proto

220 n-associated glycoprotein (MAG) binds to the nerve cell surface and inhibits nerve regeneration.

221 These data implicate the nerve cell surface gangliosides GD1a and GT1b as functio

222 We identify the nerve cell surface gangliosides GD1a and GT1b as specifi

223 neurite outgrowth is influenced by specific nerve cell surface gangliosides, which are sialic acid-c

224 tically modifying the terminal structures of nerve cell surface gangliosides; and (iv) adding highly

225 The nerve cell surface ligand(s) for MAG are not established

226 However, the problems of nerve cell survival after a proximal axotomy, difficulty

227 Signaling at nerve cell synapses is a key determinant of proper brain

228 al regulators of neurotransmitter release at nerve cell synapses.

229 to the progressive dysfunction and death of nerve cells that are responsible for the storage and pro

230 This reflects its persistence in nerve cells that connect to the mouth, nose, eye, and fa

231 ls but is present at high levels in afferent nerve cells that innervate hair cells.

232 Glutamate kills nerve cells that lack ionotropic glutamate receptors via

233 Nerve cells that re-enter a cell cycle will die rather t

234 Moreover, peripheral nerve cells that rely on microtubules to shuttle cargo a

235 ion, the virus remains inactive or latent in nerve cells that sense the region where that infection o

236 iological properties, as compared with other nerve cells, that challenge many long-standing assumptio

237 h inhibitors accumulated in the cytoplasm of nerve cells, the majority of which contained inclusions

238 of their ability to block depolarization of nerve cells, the saxitoxins exert the toxic effects asso

239 transmitters is a ubiquitous mechanism among nerve cells, the signaling pathways involved are not wel

240 Synapses, the junctions between nerve cells through which they communicate, are formed b

241 ze the steps underlying sensitization of the nerve cells to neurotoxicity when Abeta-target receptors

242 ritical regulatory factor in the response of nerve cells to oxidative stress and in the control of th

243 ization of components in this pathway allows nerve cells to target organelle delivery to specific sub

244 phenomena provide a different perspective on nerve cells to that based on chemical and electrical exc

245 xonal transport and spread of the virus from nerve cells to the skin.

246 show for the first time that amalgam causes nerve cell toxicity in culture.

247 inhibition of neurite outgrowth varied with nerve cell type.

248 oted by coculture with other embryonic optic nerve cell types but not with purified embryonic retinal

249 se-labeling experiments from three different nerve cell types, and also agree with stochastic simulat

250 d inhibition of neurite outgrowth from three nerve cell types, dorsal root ganglion neurons (DRGNs),

251 thelial cells, but not other embryonic optic nerve cell types, strongly induce the differentiation of

252 of the movement of microtubules in cultured nerve cells using a modified fluorescence photobleaching

253 Production of neurospheres from auditory nerve cells was stimulated by acute neuronal injury and

254 In NGF-differentiated PC12 catecholaminergic nerve cells, we show that de novo expressed p25alpha co-

255 One example is transport in a nerve cell, where small groups of motor proteins, such a

256 the toxin from reaching the target sites on nerve cells, where an additional layer of resistance (kd

257 itute major cell surface determinants on all nerve cells, where they contribute to cellular diversity

258 nase reversed MAG-mediated inhibition in all nerve cells, whereas a peptide inhibitor of the transduc

259 Catecholamine nerve cells which synthesize these aldehydes die in dege

260 ulate that functional disorders of vasomotor nerve cells, which originate in the embryonal neural cre

261 napses, however, are among a select group of nerve cells whose presynaptic Ca(2+)-dependent secretion

262 ells called oligodendrocytes, which wrap the nerve cells with a fatty layer called myelin.

263 d hairs, nerve density or the interaction of nerve cells with the touch domes.