ライフサイエンスコーパス: S-cone

1 S cone opsin appears last, and all opsins reach the reti

2 S cone signals influenced responses with the same sign a

3 S cone stimuli produced robust, direction-selective resp

4 S cones cover 90% of the retina by Fwk 19.

5 S cones were absent in Allocebus trichotis and Cheirogal

6 S-cone ERGs were abnormal in 50% of both groups.

7 S-cone ERGs were elicited using adaptation to 650-nm lig

8 S-cone terminals, identified by staining for S opsin, sh

9 S-cones constitute between 10% and 20% of all cones, the

10 S-cones in the cat retina do not form a regular geometri

11 e may be due in part to larger cells with an S cone phenotype in place of rods that failed to differe

12 to melanopsin, but there is evidence for an S-cone contribution as well [7, 8].

13 nding zone at 200-microm eccentricity has an S-cone density averaging 25%, but, by 800 microm, this h

14 observed that Pias3 directly regulated M and S cone opsin expression by modulating the cone-enriched

15 Although both M and S cone opsins mistrafficked as reported previously, misl

16 es due to the variable strength of L, M, and S cone input across the receptive field.

17 le L and M cone b-wave activity in ESCS, and S cones may usurp both the space and neural pathways of

18 t governs the relative numerosity of L/M and S cones.

19 re noted in the indices of recovery of M and S cones.

20 a that receive combined input from L, M, and S cones.

21 the relative contribution of melanopsin and S cones, with their overlapping, short-wavelength spectr

22 ually sensitive to the MID in achromatic and S-cone IOVD stimuli.

23 imilar healthy subjects under achromatic and S-cone isolation conditions.

24 , we used fMRI to examine how achromatic and S-cone signals contribute to human MID perception.

25 -fold reductions in the mRNAs for M-cone and S-cone opsin, respectively, whereas there was no signifi

26 ity, we studied the effects of luminance and S-cone adaptation on variability in S-cone increment thr

27 a more balanced ratio between luminance and S-cone adaptation than is used for SWAP.

28 nd-site polarization (ratio of luminance and S-cone adaptation; log [Td/Td(S)]).

29 nputs primarily from cones with mixed M- and S-cone pigments.

30 Responses to M- and S-cone stimuli usually aligned, suggesting that these ce

31 On-Off and S-cone ERGs were performed in most adults.

32 explanation based on intrusion from rod- and S-cone-driven responses.

33 he vector, CNGB3 was detected in both M- and S-cones and resulted in increased levels of CNGA3, incre

34 and with stimuli that silenced the rods and S-cones, excluded an explanation based on intrusion from

35 tions labeled with biotinylated PNA and anti-S cone opsin.

36 om rod photoreceptors, with the same sign as S cone input.

37 these bipolar cells are twice as numerous as S cones.

38 es synaptic contact with both L/M as well as S-cone photoreceptors and only minimal contact with rod

39 eved and is of considerable interest because S-cones are the basis for the primordial mammalian chrom

40 imetry, possibly due to an imbalance between S-cone adaptation and long (L)- and medium (M)-wavelengt

41 dy of goldfish red (L), green (M), and blue (S) cones, finding with microspectrophotometry widely dif

42 ntly with opsin in both S and L/M cones, but S cones express peripherin and opsin 1 to 3 weeks before

43 and super-normal cone function, mediated by S cones.

44 es, which depend on the SC, can be driven by S-cone input.

45 c inputs differs substantially: in S+ cells, S-cone signals were usually opposed by those of L- and M

46 modulates calcium conductance in the center S cone.

47 e "S-OFF" midget cells have a characteristic S-cone spatial signature, but demonstrate heterogeneous

48 pressed L/M cone opsin, and some coexpressed S cone opsin.

49 ee area, but data are conflicting concerning S-cone numbers in the adult Macaca monkey fovea, and lit

50 projections from short-wave-sensitive cones (S cones), and, consistent with this, we found that irrel

51 Short-wavelength-sensitive cones (S-cones) in the retina make little or no contribution to

52 ile comparable losses are not seen in cones, S-cones comprise less than 10% of the cone population, s

53 In contrast, S cone density was very low in central retina (0-300/mm(

54 In contrast, S-cone pedicles, with more synaptic ribbons, active zone

55 of S cones onto both types could contribute S-cone input for cortical areas primary visual cortex an

56 etina have the potential to follow a default S-cone pathway and reveal an essential role for Tr beta

57 and the developmental mechanisms determining S-cone topography are markedly different from the time t

58 NR2E3 in cone precursors and differentiating S-cones of wild-type retina also generated rod-like cell

59 ive +S and -(L+M) receptive fields, and each S cone contributes different weights to different BY gan

60 Like neighboring cones, each S cone contacts its own OFF midget bipolar cell via tria

61 However, for each S cone in macaque fovea, there are two S-cone ON bipolar

62 Overall, each S cone diverges to approximately six BY ganglion cells,

63 (Specifically, each S cone is presynaptic to four inner S-cone bipolar cells

64 Moreover, each S-cone OFF midget bipolar cell has a synaptic terminal i

65 one inherited retinal disorder, the enhanced S cone syndrome (ESCS), shows increased visual function,

66 Enhanced S-cone syndrome (ESCS) forms part of the differential di

67 Enhanced S-cone syndrome (ESCS), featuring an excess number of S

68 Enhanced S-cone syndrome has a highly variable phenotype with rel

69 Enhanced S-cone syndrome has more pleiotropy than previously appr

70 pe of retinal degeneration known as enhanced S-cone syndrome, where patients have a 30-fold increase

71 a in Nrl-knockout mice that exhibit enhanced S-cone function.

72 oroidal neovascularization (RCN) in enhanced S-cone syndrome (ESCS).

73 e is a naturally occurring model of enhanced S-cone syndrome, Goldman-Favre syndrome and clumped pigm

74 e is the rd7/rd7 retina, a model of enhanced S-cone syndrome, Goldman-Favre syndrome, and clumped pig

75 excess blue cones and loss of rods: enhanced S-cone syndrome (ESCS) in humans and rd7 in mice.

76 the loss of functional Grk1 on the enhanced S-cone Nrl(-/-) background exacerbates age-related cone

77 The recapitulation of the enhanced S-cone phenotype in retinal organoids generated from a p

78 one inherited retinal disease, the enhanced S-cone syndrome (ESCS), manifests a gain in function of

79 urse of homozygosity mapping of the enhanced S-cone syndrome gene, resulting from (1) unexpected alle

80 nduscopic findings in patients with enhanced S-cone syndrome (ESCS) may help clinicians in diagnosing

81 mouse ortholog are associated with enhanced S-cones and retinal degeneration.

82 to evoke identical activation kinetics, ESCS S cones deactivated much more slowly than ESCS or normal

83 It was postulated that in ESCS, S cones may partially replace L and M cones centrally an

84 -face electron microscopy to show that every S cone in the parafoveal retina synapses principally wit

85 ced excess M cones in contrast to the excess S cones in Nrl(-/-) mice.

86 l cell-fate determination, leading to excess S cones at the expense of other photoreceptor subtypes.

87 ellular cells and cells receiving excitatory S-cone input but not in parvocellular cells or those rec

88 ity of 10%, with several areas lacking a few S cones that are not coincident with the area of highest

89 as 100% for L and M cone tests and 99.8% for S cones.

90 hought, that the potential image quality for S cones is comparable to that for L and M cones, and tha

91 uning curve and more bandpass, than that for S-cone modulation.

92 We found S cone responses only in areas V1 and V2/V3 (peak freque

93 Each foveal S cone diverges to four S-cone ON bipolar cells but contacts them unequally, pro

94 Each foveal S cone diverges to four S-cone ON bipolar cells but cont

95 been used to determine the pattern of foveal S cones in both the fetal and adult Macaca and human.

96 ll have a distribution and density of foveal S cones similar to adults, although the high-density rin

97 Foveal S-cone increment thresholds were measured on adapting ba

98 Similarly, signals from S cone-initiated probes were altered by background chang

99 Curiously, rods did not derive from S cones in zebrafish.

100 ed interneurons that combine excitation from S cones and inhibition from L and M cones.

101 tratified cells, which receive ON input from S cones, fired synchronously with ON parasol and midget

102 ) cells and neurons that received input from S cones.

103 e either excitatory or inhibitory input from S cones.

104 tomical evidence for a synaptic pathway from S cones to OFF midget ganglion cells through OFF midget

105 e tracing validated the genesis of rods from S cones.

106 and M cones but are opposed by signals from S cones in control of the pupil.

107 lue-ON cells receive ON-type excitation from S-cones, and OFF-type excitation from ML-cones.

108 ys: one type receives input exclusively from S-cones, two types receive mixed S/M-cone input and the

109 f neurons that receive excitatory input from S-cones ("S+").

110 f neurons that receive inhibitory input from S-cones ("S-") are quite unlike those of neurons that re

111 ded from neurons with substantial input from S-cones and found that, on several important dimensions,

112 n individuals lacking L and M cone function (S cone monochromats).

113 ors fated to be rods develop into functional S-cones similar to the human NR2E3 disease.

114 ack M cones and rods, respectively, but gain S cones.

115 paradoxical dilation of the pupil to greater S-cone photon capture.

116 The highest S-cone densities are found in three distinct locations:

117 However, S-cone responses and light-dependent cGMP hydrolysis wer

118 Although the topography of human S cones is known, the human L- and M-cone submosaics hav

119 All subjects had nearly identical S-cone densities, indicating independence of the develop

120 and their blood supply which likely impacts S-cone function.

121 her weak or silent during photopic vision in S cone monochromats.

122 totransduction proteins are not expressed in S cones until 1 to 3 weeks after the appearance of S ops

123 Lack of both GRK1 and GRK7 in S cones of patients with ESCS results in a more pronounc

124 n L cones, ~3% in M cones, and negligible in S cones.

125 ng inputs differs for signals originating in S cones versus L and M cones; notably, S-cone signals ap

126 ent of opsin expression which takes place in S cones a month before M/L cones.

127 n retina and relatively higher expression in S-cone-like photoreceptors of Nrl-knockout retina compar

128 e, where patients have a 30-fold increase in S-cone sensitivity compared to normal.

129 ance and S-cone adaptation on variability in S-cone increment thresholds.

130 one subtype, but-surprisingly-an increase in S-cones.

131 neration rd7 mutant mouse leads to increased S-cones accompanied by rod degeneration, whereas ectopic

132 Inputs from individual S cones differed in strength, indicating different synap

133 al patterns revealed locations of individual S cones in BY cell receptive fields.

134 This glycinergic inhibitory S-cone amacrine cell is ideally placed for driving blue-

135 cellular cells or those receiving inhibitory S-cone input.

136 ly described by others, here termed an inner S-cone bipolar cell.

137 /M-cone signals are conveyed mainly by inner S-cone bipolar cells.

138 ly, each S cone is presynaptic to four inner S-cone bipolar cells; in turn, each bipolar cell provide

139 n cell receives input from two or more inner S-cone bipolar cells and thereby collects signals from t

140 arent functional transformation of rods into S cones in the Nrl-/- retina.

141 esponse to equiluminant stimuli that isolate S-cone activity, whereas the shortest are generated by s

142 by measuring neural responses to isoluminant S cone signals in extrastriate area MT of the macaque mo

143 responses were better driven by isoluminant S-cone inputs.

144 may result from defective development, known S cone fragility, or abnormal maintenance of mature phot

145 detached cat retina, the density of labeled S-cone outer segments (OS) decreases rapidly as early as

146 entral zone about 100 microm wide that lacks S cones and is surrounded by a ring in which the S-cone

147 log troland (Td) and from -0.16 to 3.66 log S-cone trolands (Td(S)).

148 d to model the effects of log luminance, log S-cone adaptation, and second-site polarization (ratio o

149 input from L- and M-cones, lacked measurable S-cone input, showed high spike discharge rates, high co

150 In Rds/Nrl double-null mice, S-cones form dysmorphic outer segments that lack lamella

151 thereby collects signals from three or more S cones.

152 d common but unequal inputs from one or more S cones.

153 Moreover, S-cone bipolar cells (SCBCs) are also skewed towards ven

154 t contribute to the low sensitivity of mouse S-cones.

155 ng in S cones versus L and M cones; notably, S-cone signals appear perceptually delayed relative to L

156 which differed exclusively in the amount of S cone excitation by almost two orders of magnitude (rat

157 The presence of S cone responses and the relative sensitivity of MT neur

158 nctions there have twice the responsivity of S cone contrast-response functions in normal controls.

159 ant lag between their expression and that of S cone opsin indicates that phototransduction proteins a

160 The convergence of S cones onto both types could contribute S-cone input fo

161 t in the center-surround receptive fields of S cones.

162 ndrome (ESCS), featuring an excess number of S cones, manifests as a progressive retinal degeneration

163 Estimates of the numbers of S cones missing in the fetal human fovea range from 234

164 pression [1,2] pointed to a possible role of S cones in addition to melanopsin.

165 We find no evidence for a role of S cones in the acute alerting and melatonin-supressing r

166 tead, showing that they are the terminals of S cones.

167 anges in SC activity depend on the amount of S-cone contrast.

168 avelength-sensitive cones, but the effect of S-cone inputs on the chromatic tuning properties of such

169 e3 is required to suppress the expression of S-cone genes during normal rod differentiation.

170 ral properties, and reflected integration of S-cone inputs via opponent, summing, and intermediate co

171 adaptation conditions with a higher level of S-cone adaptation and/or a more balanced ratio between l

172 s lower for conditions with higher levels of S-cone adaptation (F = 9.04, P = 0.013, for the trained

173 response to rod signals at higher levels of S-cone illumination cannot be eliminated.

174 antly reduced due to a delayed maturation of S-cone to OFF cone bipolar signaling.

175 However, the axon terminals of S-cone photoreceptors were found to express both VGLUT1

176 We conclude that the use of S-cone stimuli is insufficient to isolate SC function in

177 Variability of S-cone increment thresholds can be reduced by using adap

178 , lead to loss of rods, increased density of S-cones and supernormal S-cone-mediated vision in humans

179 age is expressed prior to the development of S-cones.

180 We conclude that excess of S-cones in the rd7 retina originate from photoreceptor p

181 ated with an approximately twofold excess of S-cones.

182 retina thickness and enhanced generation of S-cones, and develop severe early onset retinal dystroph

183 The number of S-cones in the inferior retinas of 4- or 6-mo-old KI;Fat

184 ently evolved L-M cone system, not the older S-cone channel.

185 These were identified as dendrites of the ON S-cone bipolar cell by immunostaining for the marker cho

186 patients, who rely on their vision from only S-cones and rods, suffer severely reduced visual acuity

187 rect a common precursor to a rod, M cone, or S cone outcome using Nrl(b2/b2) "knock-in" mice that exp

188 s of colored letters visible only to L, M or S cones in decreasing steps of cone contrast to determin

189 ence for multiple opsin types within rods or S cones, but immunohistochemistry and partial bleaching

190 toresponses initiated by either rhodopsin or S-cone opsin, and 3) exhibited similar light-activated t

191 express functional Cre-recombinase in M- or S-cones were established in this study.

192 recombinase was functionally active in M- or S-cones.

193 or indeed the magnocellular pathway, as our S-cone stimuli were invisible to this channel also.

194 Adult monkey foveas have an overall S-cone foveal density of 10%, with several areas lacking

195 t- wavelength sensitive cone photoreceptors (S-cones) did not show the adaptive response, and we foun

196 mounts demonstrated the preservation of PNA, S-cone, and rod opsin antibody labeling in the detachmen

197 ow that, in these two trichromatic primates, S-cone distribution and the developmental mechanisms det

198 tor beta lose rods but overproduce primitive S cones that lack outer segments.

199 es to the light signaling pathway to produce S-cone responses.

200 Second, to pure S-cone modulation, S+ cells are twice as sensitive as S-

201 We found that red-green cells received S-cone input, which aligned with M input, and, unlike bl

202 ral other rare midget RGC subtypes receiving S-cone input, but their role in color and spatial vision

203 y TVI curve, but an increase in the relative S-cone illuminance had no effect.

204 fibrillary acidic protein (GFAP), rhodopsin, S-cone opsin, and M/L-cone opsin were performed, as were

205 However, rods, S-cones, and M-cones activate the ON and OFF circuits vi

206 was tested in a Posner cueing task, the same S-cone stimuli had normal attentional effects, in that t

207 age under photopic achromatic and selective S-cone conditions in peripheral vision and whether any a

208 sible only to the short-wavelength-sensitive S cones interfere with shifts of visual attention but no

209 repression of a short wavelength-sensitive (S) cone differentiation program.

210 d from a blue or short wavelength-sensitive (S) cone On bipolar cell.

211 able analysis of short-wavelength-sensitive (S) cone responses has yet to be achieved and is of consi

212 ave sensitive (M/L) and shortwave sensitive (S) cones in most species, indicating at least dichromati

213 timuli visible only to short-wave-sensitive (S) cones.

214 of the noise in short wavelength-sensitive (S) cones arose in a later stage of the transduction casc

215 ined whether the short-wavelength-sensitive (S) cones contribute to the neuroendocrine response to li

216 kinetics of ESCS short-wavelength-sensitive (S) cones, when compared with normal L/M cone responses e

217 rs are driven by short-wavelength-sensitive (S) cones.

218 the sparsity of short-wavelength-sensitive (S) cones.

219 ed by an unknown short-wavelength-sensitive (S)-cone circuit [6].

220 he assessment of short-wavelength-sensitive (S)-cone visual function, but has also been shown to have

221 ganglion cells, one is dominated by a single S cone and one is diffusely driven by several.

222 Here, we confirm the existence of the single S-cone center OFF midget RGC circuit in the central reti

223 agree that the adult human fovea has a small S cone-free area, but data are conflicting concerning S-

224 ive in a therapeutic setting in which strong S-cone transgene expression is required.

225 increased density of S-cones and supernormal S-cone-mediated vision in humans.

226 smaller and briefer dim flash response than S cones.

227 e; L/M cones are more severely affected than S-cones.

228 n of primary visual cortex demonstrated that S cone signals were feedforward in nature and did not ar

229 Critically, however, we found that S cone stimuli did not cause IOR when saccadic eye movem

230 S, L, and M cones in these regions and that S cones may feed into different neural pathways in the c

231 We found that S cones generate slower light responses than L and M con

232 A quantitative analysis suggests that S cones provided about 10% of the input to these cells,

233 hy are markedly different from the time that S cones are first detected.

234 ance signals, leading to the conclusion that S-cone stimuli should be invisible to SC neurons.

235 The possibility that S-cone stimulation desensitizes the response to rod sign

236 The premise that S-cone stimuli are invisible to the SC has been used in

237 We propose that S-cone metabolism is less flexible than in their M/L cou

238 ion of short-wavelength light, suggests that S-cone contributions to this ganglion cell's coextensive

239 lated cone loss in either cone type and that S-cones are as regularly distributed in old as young pri

240 The S cone monochromats have clear motion-responsive regions

241 transduction within the outer segment of the S cone.

242 eady present in the synaptic terminal of the S cone.

243 The S cones in the other species and the M/L cones in all sp

244 t not by background changes seen only by the S cones.

245 We specifically examined the S cones since the previously published action spectra fo

246 es were altered by background changes in the S cones, but not by background changes in the L and M co

247 The opposition of the S cones is revealed in a seemingly paradoxical dilation

248 In the Microcebus species, the S cones had an inverse topography with very low densitie

249 The S-cone and melanopsin photoreceptor channels were found

250 The S-cone PhNR was the most sensitive test and provided the

251 The S-cone terminal thus constitutes the first critical locu

252 ing to a pressure-related mechanism, and the S-cone PhNR was the most sensitive test.

253 nent motion signal optimally conveyed by the S-cone pathway may provide a substantial contribution to

254 nge of lights used in these experiments, the S-cone system apparently does not.

255 Similar functions were generated for the S-cone pathway (isolated using Stiles' two-color thresho

256 being consistent with that expected for the S-cone submosaic.

257 ic genes while simultaneously inhibiting the S-cone pathway through the activation of Nr2e3.

258 upports the hypothesis that, in mammals, the S-cone lineage was recruited via the Maf-family transcri

259 Identification of the S-cone amacrine cell provides the missing component of a

260 econstructed the neurons and synapses of the S-cone connectome, revealing a novel inhibitory interneu

261 Colour discrimination studies show that the S-cone pathway is selectively affected by age and diseas

262 nes and is surrounded by a ring in which the S-cone density is 8%.

263 These S-cone terminals are smaller and contain more synaptic r

264 This S cone-free zone is detectable at fetal week 15.5 (Fwk15

265 This S-cone amacrine cell makes highly selective inhibitory s

266 Identifying this S-cone circuit is particularly important because ipRGCs

267 nd the relative sensitivity of MT neurons to S cone and luminance signals agree with functional magne

268 Responses to S cone (blue-yellow) and L + M cone (luminance) patterns

269 lar neurons were unequivocally responsive to S cone-isolating stimuli.

270 rrelevant peripheral stimuli visible only to S cones did not produce the saccadic distractor effect p

271 Extensive diffuse damage to S-cone bipolar and bistratified ganglion cells appears t

272 parison, they were relatively insensitive to S-cone CD.

273 s that differ in color (i.e., ratio of L- to S-cone opsin activation) while providing identical melan

274 Fourth, red-green cells often responded to S-cone stimuli.

275 erties of V1 layer 2/3 neurons responsive to S-cone stimulation.

276 Such a unique true S-cone and SCBC connecting pattern forms a basis for mou

277 In addition, true S-cones in the ventral retina form clusters, which may a

278 g patterns matching the distribution of true S-cones.

279 We found, unexpectedly, that 'true S-cones' (S-opsin only) are highly concentrated (up to 3

280 ipolar cell provides central elements to two S cones.) These bipolar cells are presynaptic to an equa

281 each S cone in macaque fovea, there are two S-cone ON bipolar cells and two blue-yellow (BY) ganglio

282 hrough inhibitory input from an undiscovered S-cone amacrine cell.

283 While these responses were unequivocal, S cone contrast sensitivity was, on average, 1.0-1.3 log

284 c features of human ESCS, including unstable S-cone-positive photoreceptors.

285 hese results demonstrate that the SC can use S-cone stimuli to guide behavior.

286 The assumption that the SC cannot use S-cone stimuli to guide behavior has never been tested.

287 nd M cones centrally and feed into the usual S cone pathways.

288 L, and second, if NRL fails to act, M versus S cone identity dictated by TRbeta2.

289 cone opsin and suppressing short-wavelength (S) cone opsin.

290 medium-wavelength (M) and short-wavelength (S) cone opsins.

291 increased approximately 2-fold, and 92% were S cones.

292 In our psychophysical experiments, when S-cone and achromatic stimuli were matched for perceived

293 ith tiny spots in the central foveola, where S cones, and thus S opponent (S(o)) cell activity, are l

294 L/M cones were regularly spaced, whereas S cones showed no regular distribution pattern.

295 To determine whether S cones contact ON and OFF midget bipolar cells as well

296 Early human NR2E3 disease with S cone hyperfunction showed thickened retinal layers wit

297 wfully modulated in contrast, and occur with S-cone stimuli invisible to the retinotectal route.

298 ient of cone distribution is disturbed, with S-cones becoming widespread across the retina.

299 ], red-green [(L - M)-cone] and blue-yellow (S-cone) modulations at various temporal frequencies.

300 In this zone, S cones were 9-14% of all cones.