ライフサイエンスコーパス: cone

1 oximately 36.8% rods and approximately 19.9% cones).

2 MS inlet by the spray that emerged from the cone.

3 increases phospho-ZBP1 levels in the growth cone.

4 ocal translation of beta-actin at the growth cone.

5 cs for reorganization at the neuronal growth cone.

6 s of the Brillouin zone (BZ) forming a Dirac cone.

7 ulation of biochemical signals within growth cones.

8 that receive nonselective input from L and M cones.

9 ic of treated and untreated rods, as well as cones.

10 e subtype, but-surprisingly-an increase in S-cones.

11 te retinae stained to distinguish S from M/L-cones.

12 ) acts as opsin phosphatase in both rods and cones.

13 elling in the L/M-cones, and lack GC1 in all cones.

14 Frizzled3 in rodent commissural axon growth cones.

15 ained by imprecision in the silencing of the cones.

16 duction or increase T3 degradation preserves cones.

17 twice as often on blue cones compared to UV cones.

18 tives, which develop separate male or female cones.

19 of them also have galactic-scale ionization cones.

20 Both rods and cones adapt to background light and to bleaches in a man

21 itive cells were absent and violet-sensitive cone and green-sensitive cone opsin positive cells were

22 We assessed the arrangements of retinal cone and rod photoreceptors in six nocturnal, three cath

23 FST permitted quantitation of cone and rod sensitivity in these patients with severe v

24 At the input level, the activation of rod/cone and suprachiasmatic nuclei (SCN) by light was parad

25 bility of cut CNS axons to form a new growth cone and then elongate.

26 psin signals are maintained independently in cones and combined at the bipolar and retinal ganglion c

27 In paired recordings of cones and horizontal cells, L-AP4 slightly reduced cone

28 a significant decrease in the number of all cones and M-cone subtype, but-surprisingly-an increase i

29 e further found that in the dorsal retina, M-cones and melanopsin contribute to dark-adapted DAC resp

30 under intermediate lighting conditions, and cones and melanopsin under bright lighting conditions.

31 synaptic transmission at ribbon synapses of cones and other retinal neurons, it is unknown whether G

32 rl disruption, rods gain partial features of cones and present with improved survival in the presence

33 tion may, therefore, disrupt the function of cones and rods in these zebrafish and cause photorecepto

34 tients, who rely on their vision from only S-cones and rods, suffer severely reduced visual acuity an

35 s, providing information about the health of cones and their relationship with the RPE, and could hel

36 timuli under conditions that target the rod, cone, and intrinsically-photosensitive (melanopsin) reti

37 f rudimentary ommatidial lenses, crystalline cones, and associated neural-like tissue within them.

38 ocalization, lack CNGB3 labelling in the L/M-cones, and lack GC1 in all cones.

39 eding filopodia formation in neuronal growth cones, and uncover a molecular heterogeneity whereby dif

40 s study was to determine the extent of rod-, cone-, and melanopsin-mediated pupillary light reflex (P

41 ic descriptors for ligand steric environment-cone angle and % buried volume-are not equivalent, despi

42 dividual parameter such as pore radius, half cone angle, and surface charges are systematically studi

43 cone behaviors.SIGNIFICANCE STATEMENT Growth cones are the motile tips of growing axons whose guidanc

44 nd UV cones, RGB cones (red, green, and blue cones) are structurally similar and unite into mirror-sy

45 receptor activation is important for growth cone assembly and axonal formation.

46 e index metamaterial induced by a Dirac-like cone at the Brillouin zone centre.

47 ic spray ionization (ESSI), forming a liquid cone at the LS interface.

48 depends on the proper balance of axon growth cone attractive and repellent cues leading axons to the

49 Single-flash cone b-wave latency and 30-Hz flicker latency responses

50 Radiographic findings from cone beam computed tomography (CBCT) and clinical sympto

51 ic sequences, perfusion computed tomography, cone beam computed tomography, single-photon emission co

52 Application of cone-beam computed tomography (CBCT) has grown exponenti

53 his systematic review is to evaluate whether cone-beam computed tomography (CBCT) imaging can be used

54 review addresses oral indications for use of cone-beam computed tomography (CBCT).

55 eolar ridge changes with and without RP with cone-beam computed tomography (CBCT).

56 Mice were imaged with Cone-Beam CT (CBCT) and irradiated (IR) to the marked ar

57 etal organization and dynamics during growth cone behaviors.SIGNIFICANCE STATEMENT Growth cones are t

58 es play a central role in controlling growth cone behaviour.

59 ure and gene expression in postmitotic mouse cones, between birth and eye opening, using serial block

60 f dopamine D1 receptors located on ON-center cone bipolar cell dendrites increases the expression and

61 onserving electrical synapses to modulate ON cone bipolar cell terminals and sign-inverting chemical

62 cell that does not require iGluRs: cone-->ON cone bipolar cell-->AII amacrine cell-->RGC.

63 receive selective UV-opsin drive from Type 9 cone bipolar cells but also mixed cone signals from bipo

64 During recovery, rod and cone bipolar cells exhibit markedly different responses

65 one cell bipolar terminals; these ON and OFF cone bipolar terminals then drive the output neurons, re

66 ic spreads, dendritic tree morphologies, and cone-bipolar connectivity patterns were restored in rege

67 t of genes is commonly expressed only in RGB cones but not in other cells.

68 upting the net assembly of MTs at the growth cone, but rather because it alters the balance of forces

69 indicates that they are driven primarily by cones, but with melanopsin (and/or rods) contributing un

70 mical (glycinergic) synapses to modulate OFF cone cell bipolar terminals; these ON and OFF cone bipol

71 up Ca(2+) when it accumulates either in the cone cell body or outer segment.

72 We show that cone cell shapes depend little on adhesion bonds and mos

73 a demonstrated that loss of Tmem30a in mouse cone cells leads to mislocalization of cone opsin, loss

74 lectroretinogram (ERG) responses and loss of cone cells.

75 lls is early onset, followed by the death of cone cells.

76 etinal analogue requires delineation also in cone cells.

77 arlier and was more significant than that in cone cells.

78 mined by the termination kinetics of the rod/cone circuits.

79 stabilizes microtubules to facilitate growth cone collapse and axon termination.

80 to inhibit endogenous EphA4-mediated growth-cone collapse induced by ephrin-B3.

81 ese findings provide insight into how growth cone collapse is regulated during axon termination in vi

82 relatively little is known about how growth cone collapse occurs prior to axon termination in vivo U

83 Growth cone collapse prior to termination is facilitated by the

84 When the LS interface was grounded the cone collapsed and the MS ion signal was lost, indicatin

85 ant and branch almost twice as often on blue cones compared to UV cones.

86 zed by a larger proportion of unequal double cones compared with the ventral retina.

87 e comparable losses are not seen in cones, S-cones comprise less than 10% of the cone population, so

88 2 x 10(5) M(-1)) because of its preorganized cone conformation.

89 h the calix-wheel adopts 1,2,3-alternate and cone conformations, which represent the kinetic and ther

90 How Shh elicits changes in the growth cone cytoskeleton that drive growth cone turning is unkn

91 fic genes, consequently preventing secondary cone degeneration.

92 The analysis revealed lower cone densities and higher rod densities in the nocturnal

93 Cone densities did not change significantly over the tre

94 OCT and ERG parameters, as well as AO-SLO cone densities, were stable during treatment.

95 that estimates of baseline RGC density from cone density are unlikely to be precise and offer little

96 the TR antagonists NH-3 and 1-850 increased cone density by 30-40% in the Rpe65(-/-) mouse model of

97 nificant association between RGC density and cone density in the normal participants, and the range o

98 Overall cone density was greater in the dorsal retina which was

99 ients than in healthy participants; however, cone density was very similar in glaucoma patients (7248

100 Retinal cone density, estimated RGC density, and cone-to-RGC rat

101 tional neural network (CNN) based method for cone detection that learns features of interest directly

102 wavelength sensitive cone photoreceptors (S-cones) did not show the adaptive response, and we found

103 receptors (NgR1, NgR2, and NgR3) are growth cone directive molecules known for inhibiting axon regen

104 RGB cone-specific transcription defines RGB cones' distinct functions for color vision.

105 mately 10%) and caused a larger reduction in cone-driven EPSCs ( approximately 30%).

106 found that an mGluR agonist (L-AP4) reduced cone-driven light responses and mEPSC frequency.

107 tina, however, the threshold intensity for M-cone-driven responses was two log units greater than tha

108 and that chromatic opponency results from M-cone-driven surround inhibition mediated by wide-field s

109 s essential for maintenance of axonal growth-cone dynamics and autophagosome turnover.

110 f the multiprotein complex regulating growth cone dynamics.

111 proliferation, radial migration, and growth cone dynamics.

112 d electrodiagnostic testing revealed rod and cone dysfunction in the 5 patients tested.

113 minance in 30% of patients, and showed a rod-cone dysfunction pattern in 20% of RP patients.

114 patients into cohorts by severity of rod and cone dysfunction.

115 patients could relate to a greater extent of cone dysfunction.

116 pigmentosa (RP), cone-rod dystrophy (CRD) or cone dystrophy (CD) harboring potential pathogenic varia

117 knockout (-/-) mice exhibited a progressive cone dystrophy accompanied by significant alterations in

118 ologic testing in 6 patients confirmed a rod-cone dystrophy phenotype.

119 CERKL deficiency in zebrafish may cause rod-cone dystrophy, but not cone-rod dystrophy, while interf

120 20-40) years, and 6 had an earlier onset rod-cone dystrophy, with a mean (range) age at onset of 12.1

121 patients, 4 had a progressive late-onset rod-cone dystrophy, with a mean (range) age at onset of 29.7

122 The latter are semimetals with Dirac/Weyl cones either not tilted (type I) or tilted (type II).

123 However, we find further variability in cone electroretinograms (ERGs) ranging from normal to ab

124 spond to the outer limiting membrane and the cone ellipsoids, respectively, separated by the cone myo

125 Cone morphology of the dogs lacking cone ERG are truncated with shortened outer and inner se

126 Immunohistochemically, cone ERG(absent) RPGRIP1 (ins/ins) retinas have extensiv

127 n increases beta-actin protein at the growth cone even when the cell bodies have been removed.

128 Actbeta reduces dynamic movements of growth cone filopodia and impairs presynaptic differentiation.

129 elopment, we examined the behavior of growth cone filopodia during the exploration of both correct an

130 ta elicit local Ca(2+) signals within growth cone filopodia that regulate axon guidance through activ

131 n of endogenous adhesion signaling to growth cone filopodia.

132 restricted angular diffusion (wobbling-in-a-cone) followed by complete orientational randomization o

133 tructure that results in the so-called Dirac cone for the ideal, perfectly ordered crystal structure.

134 Analysis of growth cone forces applied to beads at low stiffness of restrai

135 The size of the double cone-free zone differed between species.

136 Only the common buzzard had a double cone-free zone in the temporal fovea.

137 We found that newly formed growth cones from axons re-emerging from an axonal injury expre

138 ngth sensitive cone photoreceptors (L- and M-cones) from adapting.

139 mine if there is an effect on rod as well as cone function and structure.

140 Both rod function and cone function were reduced in children born extremely pr

141 hat switched on contained genes relevant for cone function.

142 romic patients, suggesting superior residual cone function.

143 ent of cytoskeleton remodeling in the growth cone (GC) during axon outgrowth and pathfinding.

144 amacrine cell that does not require iGluRs: cone-->ON cone bipolar cell-->AII amacrine cell-->RGC.

145 In the Microcebus species, the S cones had an inverse topography with very low densities

146 Three proteins found in human cones, i.e. long-wavelength (L)-, middle-wavelength (M)-

147 and horizontal cells, L-AP4 slightly reduced cone ICa ( approximately 10%) and caused a larger reduct

148 s and healthy participants underwent in vivo cone imaging at 4 locations of 8.8 degrees eccentricity

149 guidance is driven by changes in the growth cone in response to gradients of guidance molecules.

150 The S cones in the other species and the M/L cones in all species had a conventional topography with

151 nd cones respond to light much like rods and cones in amphibians and mammals.

152 The function of rods and cones in children born extremely preterm has not yet bee

153 with properties much like those of rods and cones in existing vertebrate species.

154 We have previously shown that rods and cones in lamprey respond to light much like photorecepto

155 actions between individual, spectrally typed cones in the central retina of human observers using ada

156 dle (M)-, and short (S)-wavelength-sensitive cones in the human parafovea (1.5 degrees eccentricity)

157 The S cones in the other species and the M/L cones in all spec

158 nscription in the red, green, and blue (RGB) cones in the retina, but not in other retinal cell types

159 nearly indistinguishable from that of native cones, indicating that Nrl is required for selective chr

160 stablish functional connections with L and M cones indiscriminately, implying that the cone-selective

161 ensities, where only synaptically driven rod/cone input activates ipRGCs, the duration of the ipRGC r

162 t the idea that horizontal cells can process cone input locally, extending the classical view of hori

163 otransduction pathway and as a relay for rod/cone input via synaptically driven responses.

164 One important signal that controls growth cones is that of local Ca(2+) transients, which control

165 e demonstrate that UNC-45A is a novel growth cone--localized, NMII-associated component of the multip

166 ases, the radiation emitted spreads along a "cone", making it impractical for most applications.

167 severe groups (both p < 0.001); (2) the mean cone-mediated PLR was reduced significantly in the moder

168 y rods under dim lighting conditions, rods/M-cones/melanopsin under intermediate lighting conditions,

169 ediated by voltage-gated ion channels in the cone membrane and acts by changing the frequency respons

170 of Kv3.4 channels effectively reduces growth cone membrane excitability, thereby limiting excessive C

171 ot effective since they did not modulate the cone membrane potential to the same extent.

172 richotis and Cheirogaleus medius, indicating cone monochromacy.

173 mprey and in amphibian or mammalian rods and cones; moreover background light shifts response-intensi

174 than wind-dispersed species, and particular cone morphologies are consistently associated with speci

175 Cone morphology of the dogs lacking cone ERG are truncat

176 ght into Ca(2+)/calpain regulation of growth cone motility and axon guidance during neuronal developm

177 However, how calpain regulates growth cone motility remains unclear.

178 nce that mediates opposing effects on growth cone motility.

179 e ellipsoids, respectively, separated by the cone myoids.

180 modulation of MTs by guidance cues in growth cone navigation but also help us to understand molecular

181 nt elongation and possibly mispositioning of cone nuclei in the retina.

182 that Kv3.4 is expressed in the axonal growth cones of embryonic spinal commissural neurons, motoneuro

183 s transiently expressed in the axonal growth cones of many types of embryonic neurons, acts to reduce

184 esampled after 19 y to test for selection on cone opsin genes.

185 nd violet-sensitive cone and green-sensitive cone opsin positive cells were present.

186 In both dichromats and trichromats, cone opsin signals are maintained independently in cones

187 termines the regeneration of mammalian green cone opsin with chromophore analogues such as 11-cis-6mr

188 mouse cone cells leads to mislocalization of cone opsin, loss of photopic electroretinogram (ERG) res

189 By selectively stimulating the two mouse cone opsins with green and UV light, we assessed whether

190 ter disks displayed excessive outgrowth, and cone outer segments were curved, with lamellae of hetero

191 er, the identification of small fragments of cone outer segments within the RPE led us to characteriz

192 AV delivered M-opsin localizes in the dorsal cone outer segments, and co-localizes with S-opsin in th

193 and ribbons are first reliably recognized in cone pedicles.

194 MT bundling, MT penetration into the growth cone periphery and close MT apposition to actin filament

195 led us to characterize the third band as the cone phagosomes located in the top of the RPE.

196 but also a RPE-independent visual cycle for cone photopigment within the neurosensory retina may con

197 ent suggest decreased optical density of the cone photopigments in the early postoperative period.

198 g decreased effective optical density of the cone photopigments.

199 inal tumor that expresses several markers of cone photoreceptor cells has been described earlier.

200 l, we identify a critical role of miR-211 in cone photoreceptor function and survival.

201 time- and dose-dependent declines in rod and cone photoreceptor functions as early as 120 days of age

202 (AOSLO) enables direct visualization of the cone photoreceptor mosaic in the living human retina.

203 Retinoblastomas can arise from cone photoreceptor precursors in response to the loss of

204 specifically investigate the development of cone photoreceptor ribbon synapses.

205 tropic glutamate receptors (mGluRs) regulate cone photoreceptor synaptic transmission, although the m

206 l evidence for synaptic transmission between cone photoreceptor terminals and ORDs suggests a novel p

207 cent studies have implicated TH signaling in cone photoreceptor viability.

208 etermined if treatment with HDACi can rescue cone photoreceptor-mediated visual function.

209 nted the long- and mid- wavelength sensitive cone photoreceptors (L- and M-cones) from adapting.

210 stent with this, short- wavelength sensitive cone photoreceptors (S-cones) did not show the adaptive

211 Retinal rod and cone photoreceptors arguably represent the best-understo

212 counting indicated relatively long surviving cone photoreceptors compared to rods.

213 The light responses of rod and cone photoreceptors have been studied electrophysiologic

214 regeneration is critical for the function of cone photoreceptors in bright and rapidly-changing light

215 Rod and cone photoreceptors support vision across large light in

216 Instead, foveal cone photoreceptors themselves exhibited slower light re

217 reduced in numbers, reconnected to undamaged cone photoreceptors with correct wiring patterns.

218 on are initiated in rod and several types of cone photoreceptors, respectively; these photoreceptors

219 ral architecture of the visual system inputs-cone photoreceptors-and visual perception and have impli

220 ondarily to the non-cell autonomous death of cone photoreceptors.

221 ds and their most closely related cell type, cone photoreceptors.

222 also act locally at the level of individual cone photoreceptors.

223 lpha-tubulin (tdEOS-tubulin) specifically in cone photoreceptors.

224 cover accurate input pathways from surviving cone photoreceptors.

225 e immunostained with antibodies specific for cones photoreceptors, bipolar cells, mitochondria, Mulle

226 We show that NCKX4 shapes the cone photoresponse together with the cone-specific NCKX2

227 g chickens to discriminate a stimulus (paper cone) placed at two locations in an arena, one associate

228 n of microtubule (MT) dynamics in the growth cone plays an important role in axon guidance.

229 cones, S-cones comprise less than 10% of the cone population, so significant loss would be undetected

230 Cone precursor-specific circuitry cooperates with pRB lo

231 cally attenuated without a documented rod or cone predominance in 30% of patients, and showed a rod-c

232 patially antagonistic surround to individual cone receptive fields, a signature inherited by downstre

233 quite different from rods and UV cones, RGB cones (red, green, and blue cones) are structurally simi

234 ntroducing Gbetagamma subunits directly into cones reduced EPSC amplitude.

235 lasma membrane, apical vesicle-rich inverted cone region, nucleus, and cytoplasm.

236 we assessed whether signals from individual cones remain isolated within horizontal cell dendritic t

237 hat Nogo receptors are membrane-bound growth cone repellent factors required for migration of axons a

238 We show that lamprey rods and cones respond to light much like rods and cones in amphi

239 Melanopsin and rod+cone responses differed in the temporal domain, and resp

240 Both groups had markedly reduced rod and cone responses, but nonsyndromic USH2A patients had 30 H

241 ce scanning electron microscopy of zebrafish cones revealed that nearly 100 mitochondria cluster at t

242 h, although quite different from rods and UV cones, RGB cones (red, green, and blue cones) are struct

243 The finding that synaptic transmission at cone ribbon synapses is regulated by Gbetagamma/SNAP-25

244 ation assays demonstrate that retinal growth cones robustly adapt towards ephrin-A/EphA forward and r

245 tosomal recessive retinitis pigmentosa (RP), cone-rod dystrophy (CRD) or cone dystrophy (CD) harborin

246 rafish may cause rod-cone dystrophy, but not cone-rod dystrophy, while interfering with the phagocyto

247 LCA), juvenile retinitis pigmentosa (RP) and cone-rod dystrophy.

248 equences; while Prph2Y/+ animals exhibited a cone-rod electroretinogram defect, Prph2Y/+/Rom1-/- anim

249 While comparable losses are not seen in cones, S-cones comprise less than 10% of the cone popula

250 M cones indiscriminately, implying that the cone-selective circuitry supporting red-green color visi

251 For most patients, the degree of rod and cone sensitivity losses showed a relationship, thereby p

252 rom Type 9 cone bipolar cells but also mixed cone signals from bipolar Types 6, 7, and 8.

253 A critical early transformation applied to cone signals is horizontal-cell-mediated lateral inhibit

254 than peripheral cones, unexpectedly linking cone signals to perceptual sensitivity.

255 ed intensity), and narrow forward scattering cone similar to giant clams.

256 Marine cone snails contain a high diversity of toxins in their

257 Cone spacing was measured in 4 patients from AOSLO image

258 Cone spacing was normal at almost all locations in 2 pat

259 ave implications for the neural locus of the cone-specific circuitry supporting color vision.

260 These cells also expressed Opn1mw, a cone-specific marker and nestin, a marker for neural pre

261 pes the cone photoresponse together with the cone-specific NCKX2: NCKX4 acts early to limit response

262 y provides a starting point to study how RGB cone-specific transcription defines RGB cones' distinct

263 port that the rainbow enhancers activate RGB cone-specific transcription of the ponli and crb2b genes

264 Recent studies show that there is sufficient cone structure remaining in the central fovea of BCM pat

265 nt decrease in the number of all cones and M-cone subtype, but-surprisingly-an increase in S-cones.

266 d acts by changing the frequency response of cones such that their responses speed up as the membrane

267 toreceptor layer can resolve ambiguity about cone survival in age-related macular degeneration.

268 Cone survival was significantly improved in Rpe65(-/-) a

269 With the transverse spin cone symmetry restricted to be two-fold, the one-step sh

270 regulate light response encoding across the cone synapse, accomplished in part by triggering G-prote

271 ut nonsynchronous expression of molecules in cone synaptic development.

272 ropic glutamate receptor (mGluR), can reduce cone synaptic transmission via Gbetagamma in tiger salam

273 etermining up to 85% of the variance in some cone system response parameters.

274 apical radiographs were taken using the long-cone technique before and after implant placement.

275 In contrast to adults, larval UV cone telodendria are more numerous (1.3 times) than blue

276 We characterized short wavelength cone telodendria in adult and larval zebrafish retina.

277 dria are more numerous (1.3 times) than blue cone telodendria.

278 dria are less abundant than short wavelength cone telodendria.

279 f the parameter that characterizes the Dirac cones: the Fermi velocity.

280 Commonly denominated Dirac cones, these dispersion relations are considered to be t

281 visual-pigment renewal in mammalian rods and cones through a non-enzymatic process involving retinyl-

282 in the normal participants, and the range of cone-to-RGC density ratios was relatively large in healt

283 nal cone density, estimated RGC density, and cone-to-RGC ratios in glaucoma patients and healthy cont

284 n termination is protracted, with the growth cone transitioning from a dynamic to a static state.

285 knockdown reduced axon outgrowth and growth cone turning in Wnt5a gradients, likely due to disorgani

286 e growth cone cytoskeleton that drive growth cone turning is unknown.

287 bited slower light responses than peripheral cones, unexpectedly linking cone signals to perceptual s

288 that targeted melanopsin separately from the cones using pulsed (3-s) spectral modulations around a p

289 led; they argue for the presence of rods and cones very early in the evolution of vertebrates with pr

290 , encode TRs; THRB2 has been associated with cone viability.

291 ting for the high temporal frequency bias of cone vision and the negative correlation between magnitu

292 respond as if punishment was likely when the cone was placed near to the punished location.

293 which visibility for melanopsin versus rods+cones was independently modulated, and we recorded evoke

294 end along the entire external segment of the cones, we do not believe them to be the structure respon

295 super resolution microscopy of fixed growth cones, we found that tau colocalizes with MTs and actin

296 oral dynamics of protein synthesis in growth cones, we further developed a technique for single molec

297 S cones were absent in Allocebus trichotis and Cheirogaleu

298 s ejected in a 30 degrees -60 degrees hollow cone, which is filled with more energetic electrons dete

299 Membrane excitability in the growth cone, which is mainly controlled by voltage-gated Ca(2+)

300 commonly and restrictively expressed in RGB cones, which largely define the beginning of the color v