ライフサイエンスコーパス: retinal neuron

1 ery few (450 in each mouse retina, 0.005% of retinal neurons).

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

3 croglia/macrophages associate with apoptotic retinal neurons.

4 ectric current to stimulate the nearby inner retinal neurons.

5 ltiple genes expressed specifically in inner retinal neurons.

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

7 nin potentiates signaling from rods to inner retinal neurons.

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

9 es and decreasing apoptosis of pericytes and retinal neurons.

10 t not genes characteristic of differentiated retinal neurons.

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

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

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

14 normal electrophysiology at the level of the retinal neurons.

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

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

17 leads to chronic but reversible silencing of retinal neurons.

18 important role in promoting the survival of retinal neurons.

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

20 or studying the function of coupling between retinal neurons.

21 and progressive loss of adult cerebellar and retinal neurons.

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

23 the activity of second-order hyperpolarizing retinal neurons.

24 unced expression in photoreceptors and other retinal neurons.

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

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

27 retinal vasculature can result in damage to retinal neurons.

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

29 n synaptic activity and AMPAR trafficking in retinal neurons.

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

31 + and the actin cytoskeleton organization in retinal neurons.

32 ot solely photoreceptor cells but also inner retinal neurons.

33 metabolism increased insulin sensitivity in retinal neurons.

34 hich are derived from the second-order inner retinal neurons.

35 CoCl(2) upregulated Hsp27 in cultured retinal neurons.

36 ), can block differentiation and function of retinal neurons.

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

38 stnatal retina, and it is expressed by inner retinal neurons.

39 ts their level of innervation by more distal retinal neurons.

40 tic connections between specific subtypes of retinal neurons.

41 d for coincidence and threshold detection in retinal neurons.

42 lved in the development of multiple types 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 d dopamine-dependent GABA release from other retinal neurons.

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

48 that are expressed in overlapping subsets of retinal neurons.

49 rriers and thereby access and photosensitize retinal neurons.

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

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

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

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

54 faster cone-driven responses in second-order retinal neurones.

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

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

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

58 ant for transgene expression in regenerating retinal neurons after eye injury.

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

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

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

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

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

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

65 munohistochemistry for bromodeoxyuridine and retinal neuron and photoreceptor-specific markers.

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

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

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

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

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

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

72 Characterization of retinal neurons and glia was performed by immunocytochem

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

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

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

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

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

78 whereas SERCA2b was found in the majority of retinal neurons and in glial cells.

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

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

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

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

83 med that MMP activity occurred only in these retinal neurons and not in glial or other retinal cell t

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

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

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

87 kb promoter directed transgene expression to retinal neurons and progenitor cells, the activity of mu

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

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

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

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

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

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

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

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

101 Cone-driven responses of second-order retinal neurons are considerably faster than rod-driven

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

103 urposes of this study were to identify which retinal neurons are infected and to determine the routes

104 Previous results suggest that retinal neurons are infected early during murine cytomeg

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

106 The mechanisms by which retinal neurons are patterned along the dorsal/ventral a

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

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

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

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

111 trolled by a hierarchy of interactions among retinal neurons, astrocytes and blood vessels.

112 expressed in calbindin- and Prox1-expressing retinal neurons at birth.

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

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

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

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

117 ds and cones, after processing by downstream retinal neurons (bipolar, horizontal, amacrine and gangl

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

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

120 signaling did not prevent differentiation of retinal neurons, but it did disrupt spatial patterning i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 hes: 1) hydrogen peroxide (H(2)O(2))-induced retinal neuron degeneration in vitro, and 2) light-induc

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

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

138 Retinal neurons differentiated, but their laminar arrang

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

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

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

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

143 Retinal neurons exhibit sustained versus transient light

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

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

146 ons adopted a generic rather than a specific retinal neuron fate.

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

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

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

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

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

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

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

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

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

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

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

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

159 nitors or Muller glia, and added dissociated retinal neurons from older retinas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 f ptc+/- mice could be induced to regenerate retinal neurons in response to damage, we bred ptc+/- mi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 e that expression of ChR2 in surviving inner retinal neurons of a mouse with photoreceptor degenerati

219 f cell apoptosis and caspase-3 activation in retinal neurons of C57Bl/6 mice within days of diabetes

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

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 Alterations in retinal neuron populations were evaluated quantitatively

230 ities is affected by the spiking activity of retinal neurons, possibly including that of the DA neuro

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

232 In sum, these results show that retinal neurons produce a cytostatic TGF(beta) signal th

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

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

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

236 Retinal neurons release platelet-derived growth factor (

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

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

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

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

241 Apoptotic inner retinal neurons, resulting from intravitreal injection o

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

243 BDNF treatment of retinal neurons results in reduced RhoA activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 In retinal neurons, the molecular chaperone sigmaR1 binds B

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

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

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

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

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

276 explore the feasibility of converting inner retinal neurons to photosensitive cells as a possible st

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

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

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

289 ll type that is distinct from other types of retinal neurons, which we termed large glucagon-expressi

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

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

292 itric oxide, GABAergic and glycinergic inner retinal neurons with expression of a reporter for the ci

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