ライフサイエンスコーパス: retinal neuron

1 (important for the high metabolic demands of retinal neurons).

2 that are expressed in overlapping subsets of retinal neurons.

3 cell death but spare second- and third-order retinal neurons.

4 ous reservoir may recover function of "sick" retinal neurons.

5 nd subsequent regeneration of HuC/D(+) inner retinal neurons.

6 ectric current to stimulate the nearby inner retinal neurons.

7 ltiple genes expressed specifically in inner retinal neurons.

8 ssion with the modulation of Src activity in retinal neurons.

9 nin potentiates signaling from rods to inner retinal neurons.

10 tion, which is necessary for the survival of retinal neurons.

11 es and decreasing apoptosis of pericytes and retinal neurons.

12 t not genes characteristic of differentiated retinal neurons.

13 a(v)1.3 L-type Ca(2+) channels in salamander retinal neurons.

14 rentiation when in the vicinity of wild-type retinal neurons.

15 s known about propofol's effects on specific retinal neurons.

16 at supports plate-shaped synaptic ribbons in retinal neurons.

17 zed in photoreceptor cells and in some inner retinal neurons.

18 l roles in processing the light responses of retinal neurons.

19 leads to chronic but reversible silencing of retinal neurons.

20 important role in promoting the survival of retinal neurons.

21 ginates mainly from activity of second-order retinal neurons.

22 or studying the function of coupling between retinal neurons.

23 and progressive loss of adult cerebellar and retinal neurons.

24 ture and interactions in the spike trains of retinal neurons.

25 the activity of second-order hyperpolarizing retinal neurons.

26 unced expression in photoreceptors and other retinal neurons.

27 c degeneration of cerebellar, brainstem, and retinal neurons.

28 le is known about the responses of the inner retinal neurons.

29 retinal vasculature can result in damage to retinal neurons.

30 (RPG) expression and the differentiation of retinal neurons.

31 n synaptic activity and AMPAR trafficking in retinal neurons.

32 n cAMP levels and PKA activity in developing retinal neurons.

33 + and the actin cytoskeleton organization in retinal neurons.

34 ot solely photoreceptor cells but also inner retinal neurons.

35 etinal imaging to understand the function of retinal neurons.

36 croglia/macrophages associate with apoptotic retinal neurons.

37 d dopamine-dependent GABA release from other retinal neurons.

38 rriers and thereby access and photosensitize retinal neurons.

39 erve to replace or resurrect dead or injured retinal neurons.

40 normal electrophysiology at the level of the retinal neurons.

41 vels in the glia, but very low levels in the retinal neurons.

42 tic connections between specific subtypes of retinal neurons.

43 and formed a cell layer connected with host retinal neurons.

44 inal homeostasis and support the survival of retinal neurons.

45 cells (MGPCs) with the ability to regenerate retinal neurons.

46 ectric current to stimulate the nearby inner retinal neurons.

47 liary body, lens epithelium, and a subset of retinal neurons.

48 mprise approximately 1/2 of a percent of all retinal neurons.

49 from reprogramming and differentiating into retinal neurons: 1) repressive chromatin in the promoter

50 on by electrically stimulating the remaining retinal neurons [2].

51 d precursor cells, whereas loss of any other retinal neurons activates Muller glia proliferation to p

52 Vision impairment caused by loss of retinal neurons affects millions of people worldwide, an

53 CANCE STATEMENT Adult zebrafish generate new retinal neurons after a tissue-disrupting lesion.

54 ller glia upregulate genes characteristic of retinal neurons after growth factor stimulation in vitro

55 n shown to be effective in transducing inner retinal neurons after intravitreal injection in several

56 and an acute treatment increased survival of retinal neurons after optic nerve crush (ONC) in rodent

57 igated to examine their abilities to protect retinal neurons against glutamate toxicity.

58 as a negative feedback mechanism protecting retinal neurons against glutamate-induced excitotoxicity

59 Dark and light adaptation of retinal neurons allow our vision to operate over an enor

60 e postsynaptic current (PSC) in second-order retinal neurons and (2) capacitance measurements of vesi

61 GFbeta signaling is important in maintaining retinal neurons and blood vessels and is a factor contri

62 ng of spontaneous activity in populations of retinal neurons and by making whole-cell recordings from

63 Many retinal diseases lead to the loss of retinal neurons and cause visual impairment.

64 c sequence of circuit models that represents retinal neurons and connections and fitted them to the e

65 a variety of diseases involving the death of retinal neurons and contributes to neurodegenerative pro

66 CX3CL1 signaling from retinal neurons and endothelial cells likely modulates d

67 s and damage to the retina lead to losses in retinal neurons and eventual visual impairment.

68 rmine that microglia primarily interact with retinal neurons and find that depletion of microglia via

69 Characterization of retinal neurons and glia was performed by immunocytochem

70 cid metabolites differentially gate TRPV4 in retinal neurons and glia, with potentially significant c

71 and an absence of terminally differentiated retinal neurons and glia.

72 these cells are responsible for regenerating retinal neurons and glia.

73 ssing Muller glia were capable of generating retinal neurons and glia.

74 ls, and an increase in phosphorylated tau in retinal neurons and glia.

75 evious studies by showing that HIF-1alpha in retinal neurons and HIF-2alpha in Muller glia play disti

76 ty of progenitor cells to differentiate into retinal neurons and is highly expressed by human Muller

77 olecule identified that is produced by dying retinal neurons and is necessary to induce Muller glia t

78 take within the retina, and are expressed by retinal neurons and Muller cells.

79 to result from a complex interaction between retinal neurons and Muller glia, which release toxic mol

80 ynthase (NOS), modulates the function of all retinal neurons and ocular blood vessels and participate

81 tion that reveals GC somas, axons, and other retinal neurons and permits their quantitative analysis.

82 3HT NPs) mediate light-evoked stimulation of retinal neurons and persistently rescue visual functions

83 o dedifferentiate, migrate, and generate new retinal neurons and photoreceptor cells by alpha-aminoad

84 ured CNS.SIGNIFICANCE STATEMENT The death of retinal neurons and photoreceptors is a leading cause of

85 and macular degeneration, cause the death of retinal neurons and profound vision loss.

86 xpressed by non-overlapping subsets of chick retinal neurons and promote their lamina-specific arbori

87 cells capable of regenerating all classes of retinal neurons and restoring visual function.

88 Ngb and Cygb are widely distributed in retinal neurons and RPE, but not in glial cells of the c

89 We apply this method to retinal neurons and show that it can accurately recover

90 ortant visual computation is accomplished by retinal neurons and synapses.

91 at insulin mediates a prosurvival pathway in retinal neurons and that normal retina expresses a highl

92 self-spacing behavior of different types of retinal neurons and the extent to which that behavior ge

93 done to achieve higher yields of functioning retinal neurons and to promote better integration within

94 Retinal neurons and vasculature interact with each other

95 The construct expressed in most inner retinal neurons, and it also suppressed visual loss and

96 of inner retinal neurons, synapse with host retinal neurons, and respond to light.

97 Mouse somatosensory neurons, retinal neurons, and taste receptor cells do not appear

98 s consistent with hypoxia in Muller glia and retinal neurons, and we find a metabolic shift that comb

99 hyperpolarizing second- and all third-order retinal neurons; and TTX (tetrodotoxin, 6 muM), to block

100 f Epo also protected against hypoxia-induced retinal neuron apoptosis.

101 re resulted in a dose-dependent reduction in retinal neuron apoptosis.

102 Individual types of retinal neurons are distributed to minimize proximity to

103 The various types of retinal neurons are each positioned at their respective

104 ge-gated sodium channels (Na(v) channels) in retinal neurons are known to contribute to the mammalian

105 Our results indicate that multiple types of retinal neurons are potential circadian clock neurons th

106 in the monkey retina and localize to diverse retinal neurons as well as putative microglia.

107 d photopic signal arose only from lost inner retinal neurons, as cone numbers did not change.

108 clock genes in individual, identified mouse retinal neurons, as well as characterized the clock gene

109 of Casz1 increases production of early-born retinal neurons at the expense of later-born fates, wher

110 portant in shaping responses of second-order retinal neurons at the tonically active photoreceptor sy

111 However, the extent to which regenerated retinal neurons attain appropriate morphologies and circ

112 NAs in terminally differentiated adult human retinal neurons based on their sequence conservation acr

113 tion, they possess the potential to generate retinal neurons, both in vitro and in vivo.

114 ors, in rod bipolar cells, and in most inner retinal neurons but was absent from cones.

115 ive in hippocampal, dorsal root ganglia, and retinal neurons, but its propermeability, vasodilatatory

116 mediate the initial proliferative arrest of retinal neurons, but may indirectly induce arrest in RPC

117 Ngb IR was localized within retinal neurons, but not in glia.

118 can signal changes in light levels to inner retinal neurons, but the role of glutamate in communicat

119 multipotent retinal stem cells that generate retinal neurons by homeostatic and regenerative developm

120 ferentiation of the photoreceptors and other retinal neurons by influencing the expression of target

121 layed rectifier potassium (K(V)) channels in retinal neurons by means of a metabotropic receptor path

122 rostheses that stimulate the remaining inner retinal neurons, bypassing degenerated photoreceptors, h

123 A subset of retinal neurons, called direction-selective ganglion cel

124 In some pairs of retinal neurons, called paramorphic, one member responds

125 Under these conditions and pathologies, retinal neurons can die via apoptosis that may be due to

126 ls, greater than the range of output signals retinal neurons can produce.

127 result in photoreceptor loss, but the inner retinal neurons can survive, making them potentially ame

128 have the additional ability to generate new retinal neurons capable of sight restoration.

129 study suggests that changes in the output of retinal neurons caused by disturbances in outer retinal

130 precise synaptic connections among distinct retinal neuron cell types is critical for processing vis

131 s have neurogenic potential and can generate retinal neurons, confirming a hypothesis, first proposed

132 esults provide a better understanding of how retinal neurons connect to the central circadian pacemak

133 Subsequently, inner retinal neurons develop aberrant synaptic activity, comp

134 We found that in the absence of microglia, retinal neurons did not undergo overt cell death or beco

135 otein, activates Atonal (Ato) expression and retinal neuron differentiation synergistically with the

136 clude that Isl1 has an indispensable role in retinal neuron differentiation within restricted cell po

137 gnificantly increased the apoptotic death of retinal neurons during embryonic and postnatal developme

138 As RD progresses, retinal neurons exhibit aberrant activity, driven by AII

139 Retinal neurons exhibit sustained versus transient light

140 In summary, retinal neurons exhibited numerous age-related quantitat

141 Dopaminergic and other inner retinal neurons express many of the clock genes, whereas

142 h have the remarkable capacity to regenerate retinal neurons following a variety of damage paradigms.

143 e a cell-autonomous requirement for ADCY8 in retinal neurons for normal midline crossing.

144 nds were also present in certain other adult retinal neurons, for example, horizontal cells and amacr

145 he absence of beta1-Integrin or Cas function retinal neurons form ectopic cell clusters beyond the in

146 ecific structure, in which specific types of retinal neurons form highly selective synapses to transf

147 However, little is known of how retinal neurons form this laminar-specific synaptic stru

148 show a simultaneous requirement for Math5 in retinal neuron formation and cell cycle progression.

149 RPE, photoreceptors, and inner retinal neurons formed normally in zebrafish platinum mu

150 tivation of the receptor by G1 protected the retinal neuron from insult, whereas G15, an antagonist o

151 demonstrate that EGCG provides protection to retinal neurones from oxidative stress and ischemia/repe

152 In retinal explants, compound 12j protected retinal neurons from high glucose-induced oxidative stre

153 ave developed efficient methods for deriving retinal neurons from human embryonic stem (hES) cells.

154 Zebrafish can regenerate retinal neurons from intrinsic stem cells, Muller glia,

155 IOP in glaucomatous mouse eyes and protected retinal neurons from IOP-induced death.

156 have a robust ability to regenerate injured retinal neurons from Muller glia (MG) that activate the

157 Responses from postsynaptic retinal neurons from the salamander Ambystoma tigrinum s

158 ogenitors differentiate primarily into inner retinal neurons (ganglion and amacrine cells), with func

159 in the promoter regions of non-photoreceptor retinal neuron genes; 2) highly-methylated promoters of

160 lacking TGF-beta receptor II (TGFbetaRII) in retinal neurons had reduced C1q expression in RGCs and r

161 These results suggest that retinal neurons have a homeostatic mechanism that integr

162 cted time to develop blindness suggests that retinal neurons have an endogenous mechanism for protect

163 to reprogram resident glial cells to replace retinal neurons have been proposed.

164 Imaging of exocytosis from isolated retinal neurons, however, has revealed ectopic release (

165 ansmission, dopamine modulates all layers of retinal neurons; however, it is not well understood how

166 markers and by the expression of markers of retinal neurons (HuD, betaIII tubulin, rhodopsin, BRN3B,

167 retinogram (ERG) via activity of third-order retinal neurons, i.e. amacrine and ganglion cells.

168 lamin B2 prevents proper lamination of adult retinal neurons, impairs synaptogenesis, and reduces con

169 of S1R in the nuclear envelope in all three retinal neurons implicates a potential role of S1R in mo

170 Baseline images of the fluorescent retinal neurons in 30 Thy1-CFP mice were obtained using

171 hich have biases toward producing subsets of retinal neurons in a terminal division, with the types o

172 Loss of retinal neurons in adult zebrafish (Danio rerio) induces

173 ng provides a trophic signal for transformed retinal neurons in culture, but the in vivo role of Akt

174 ng provides a trophic signal for transformed retinal neurons in culture, but the role of IR activity

175 f the overexpression of alpha-crystallins in retinal neurons in culture.

176 tigated in two animal models of diabetes and retinal neurons in culture.

177 ion and significantly decreased apoptosis of retinal neurons in embryos and pups.

178 e every 2 weeks totalling 5-6 injections) to retinal neurons in Ins2(Akita) diabetic mice.

179 xels provide highly localized stimulation of retinal neurons in rats.

180 GFP) (Chop2-GFP) were evaluated in the inner retinal neurons in the common marmoset Callithrix jacchu

181 3) were detected primarily in differentiated retinal neurons in the embryonic and adult retina.

182 Subsequently, the number of fluorescent retinal neurons in the group that received one treatment

183 In contrast, the number of fluorescent retinal neurons in the group that received repeated brim

184 expression of ChR2 was observed in the inner retinal neurons in the marmoset retina through intravitr

185 report that HDAC4 regulates the survival of retinal neurons in the mouse in normal and pathological

186 As most of fluorescent retinal neurons in this system are RGCs, these findings

187 rce of stem cells is important for producing retinal neurons in three-dimensional (3D) organ cultures

188 morphology and failed to differentiate into retinal neurons in vitro or in vivo.

189 tant role in adult hMSC differentiation into retinal neurons in vitro.

190 retina has the potential to regenerate inner retinal neurons in vivo.

191 in-2 (ChR2), can be achieved in rodent inner retinal neurons in vivo.

192 oping mice studied, we detected infection of retinal neurons; in many mice, this was also associated

193 op2-GFP was observed in all major classes of retinal neurons, including all major types of ganglion c

194 d by the upregulation of specific markers of retinal neurons, including betaIII tubulin, rhodopsin, B

195 an extensive gap junction network with other retinal neurons, including other ipRGCs, which shapes th

196 ) channels play important roles in mammalian retinal neurons, including photoreceptors, bipolar cells

197 ging from focal lesions with displacement of retinal neurons into subretinal space to severe hypocell

198 rhodopsins, such as ChR2, in surviving inner retinal neurons is a potential strategy for the restorat

199 Regenerating retinal neurons is a therapeutic goal.

200 In vitro culture of dissociated retinal neurons is an important model for investigating

201 Therefore, although the Sema3E secreted by retinal neurons is evenly distributed throughout the ret

202 hows that extrinsic feedback from developing retinal neurons is important for the temporal expression

203 ulated crosstalk between the vasculature and retinal neurons is increasingly recognized as a major fa

204 ission at ribbon synapses of cones and other retinal neurons, it is unknown whether Gbetagamma contri

205 their ability to up-regulate genes found in retinal neurons, it was concluded that these sphere-form

206 This protocol can also be applied to study retinal neurons labeled with other two photon-excitable

207 Retinal neuron loss in Grn-KO mice is preceded by nuclea

208 gs may aid in designing therapies to restore retinal neurons lost to degenerative diseases.

209 x36) subunits, which are highly expressed by retinal neurons, markedly reduced loss of neurons and op

210 ngs indicate that On-Off direction-selective retinal neurons may have evolutionarily diverged in prim

211 constitutive expression of SOCS6 protein in retinal neurons may improve glucose metabolism, while el

212 nal progenitor cells that differentiate into retinal neurons, mimicking the responses observed in the

213 By use of protocols that preserve proximal retinal neuron morphology, we have examined the shape, d

214 In response to loss of retinal neurons, Muller glia partially dedifferentiate,

215 LIRD rapidly triggered retinal neuron neuritogenesis and up-regulated several k

216 n preparing the eye for vision by regulating retinal neuron number and initiating a series of events

217 by a light-response pathway that suppresses retinal neuron number, limits hypoxia and, as a conseque

218 To establish functional circuitry, retinal neurons occupy spatial domains by arborizing the

219 n effectively restore OFF responses in inner retinal neurons of mice with retinal degeneration.

220 t of large numbers of GCs onto the remaining retinal neurons of the same class.

221 t of large numbers of GCs onto the remaining retinal neurons of the same class.

222 inst loss of fluorescence within fluorescent retinal neurons of Thy1-CFP mice after optic nerve crush

223 operational range of rod bipolar cells, the retinal neurons operating immediately downstream of rod

224 r processes but no characteristics of mature retinal neurons or glia.

225 adult retinal architecture, the survival of retinal neurons, or the laminar organization of their de

226 ferred expression of this isotype in certain retinal neurons plays a cell specific role, or whether i

227 m that is essential for targeting a discrete retinal neuron population to the proper lamina.

228 Most inner retinal neuron populations responded to kainate in a con

229 pressing channel rhodopsin-2 (ChR2) in inner retinal neurons, previous studies have demonstrated rest

230 Electrical stimulation of surviving retinal neurons provides an alternative route for the de

231 e light-dependent activation of spared inner retinal neurons, recovering subcortical, cortical and be

232 ows that after selective ablation, zebrafish retinal neurons regenerate and reconstruct some, althoug

233 , after a chemical lesion that ablates inner retinal neurons, regenerated retinal bipolar neurons (BP

234 In addition, we found that retinal neurons remain immature for prolonged periods of

235 ontrast, the mean proportions of fluorescent retinal neurons remaining in the group treated with MS-2

236 The mean proportions of fluorescent retinal neurons remaining in the vehicle group following

237 Milner and Do describe how the population of retinal neurons responsible for entrainment of the brain

238 Apoptotic inner retinal neurons, resulting from intravitreal injection o

239 onged light sensitivity on multiple types of retinal neurons, resulting in synaptically amplified res

240 c nerve crush, the proportion of fluorescent retinal neurons retaining fluorescence was 44+/-7% of ba

241 rafish line, in which all different types of retinal neurons show distinct fluorescent spectra, we fo

242 nal deletion of TGF-beta-inhibiting Smad7 in retinal neurons significantly enhanced Smad3 phosphoryla

243 nes associated with neurogenesis, as well as retinal neuron-specific genes, are differentially expres

244 on.SIGNIFICANCE STATEMENT Different types of retinal neuron spread their processes across the surface

245 and Sema5B constrain neurites from multiple retinal neuron subtypes within the inner plexiform layer

246 , but rather to the cell lineage (early born retinal neurons) suggesting that the expression of class

247 ersistence of transcripts expressed by inner retinal neurons suggests that despite significant plasti

248 postmitotic, terminally differentiated adult retinal neurons suggests that EGFR has pleiotropic funct

249 and G9a-mediated HKM plays crucial roles in retinal neuron survival and may represent novel epigenet

250 authors reveal a role for HKM in regulating retinal neuron survival.

251 MG-derived neurons express markers of inner retinal neurons, synapse with host retinal neurons, and

252 isual circuit is topographic [5, 6], wherein retinal neurons target and activate predictable spatial

253 r for VEGF, was more abundantly expressed in retinal neurons than in endothelial cells, including end

254 rabbit AII amacrine cell, a multifunctional retinal neuron that forms an electrically coupled networ

255 glaucoma are disorders that target specific retinal neurons that can ultimately lead to vision loss.

256 sh (Danio rerio) are capable of regenerating retinal neurons that have been lost due to mechanical, c

257 mine activates a receptor in adult mammalian retinal neurons that is distinct from classical D1 and D

258 genesis is indicated by increased early-born retinal neurons that result from accelerated cell cycle

259 i-bullwhip cells are unconventional types of retinal neurons that utilize the neuropeptides glucagon,

260 s of Sfrs1 function resulted in the death of retinal neurons that were born during early to mid-embry

261 Although NGB is greatly expressed in retinal neurons, the biological functions of NGB in reti

262 The second-order retinal neurons, the bipolar cells, are thought to initi

263 In retinal neurons, the molecular chaperone sigmaR1 binds B

264 own to modulate the number of other types of retinal neuron-the proapoptotic gene, Bax, and tyrosinas

265 about flicker-induced changes of activity of retinal neurons themselves.

266 ferating resident stem cells, which generate retinal neurons throughout life.

267 eceives information from a similar number of retinal neurons, throughout the visual field.

268 ntenance of retinal polarity and survival of retinal neurons, thus providing the basis for the pathol

269 d unprecedented cellular regulation of VEGF: retinal neurons titrate VEGF to limit neuronal vasculari

270 erently rely on the ability of the remaining retinal neurons to correctly synapse with new photorecep

271 cessary to better understand the response of retinal neurons to electric stimulation.

272 ly with the spatio-temporal sensitivities of retinal neurons to encode spatial information.

273 gonistic center-surround receptive fields of retinal neurons to enhance visual contrast.

274 this enhances signal transmission from inner retinal neurons to ganglion cells, potentially allowing

275 etic retina, increases the susceptibility of retinal neurons to injury in the presence of increased c

276 ation and fractionation METHODS: Survival of retinal neurons to metabolic stress after overexpression

277 Converting inner retinal neurons to photosensitive cells by expressing ch

278 uthors have genetically engineered surviving retinal neurons to take on the lost photoreceptive funct

279 trols match the effective signaling range of retinal neurons to the local image statistics.

280 these agents to examine the contribution of retinal neurons to this syndrome.

281 e studied the effects of aerobic exercise on retinal neurons undergoing degeneration.

282 Whereas many retinal neurons use L-type channels to stimulate vesicle

283 Retinal neurons use multiple strategies to fine-tune vis

284 However, it is not known how adult mammalian retinal neurons use Thy1.

285 Reprogramming retinal neurons using this protocol will take 56 d, and

286 l rh-NGF exhibits neuroprotective effects on retinal neurons via influencing secondary degeneration p

287 ncrease in glucosylceramide composition, R28 retinal neurons were treated with glucosylceramide synth

288 Excitatory inputs to inner retinal neurons were visualized by introduction of a pla

289 ated whether trafficking of AMPARs occurs in retinal neurons, which are subject to tonic glutamate re

290 , leading to blindness, but spare downstream retinal neurons, which can be targeted for optogenetic t

291 Electrical stimulation of retinal neurons with an advanced retinal prosthesis may

292 etinal photoreceptors by directly activating retinal neurons with electrical stimulation.

293 ion cells (RGCs) are the best studied of the retinal neurons with respect to the effect of diabetes.

294 during the critical period in development of retinal neurons with small, foveal receptive fields.

295 Incubation of live retinal neurons with TRPM1-positive MAR serum resulted i

296 ted alternative splicing for the survival of retinal neurons, with sensitivity defined by the window

297 Loss of fluorescent retinal neurons within specific retinal areas was determ

298 the retina, not hitherto shown, in discrete retinal neurons within the inner retina.

299 ification of the size of every population of retinal neuron, yet genetic variants work largely indepe

300 he formation of the antagonistic surround of retinal neurons, yet the mechanism by which horizontal c