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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 cone stimuli suppress glutamate release onto metabotro
5                                              S cones cover 90% of the retina by Fwk 19.
6                                              S cones were absent in Allocebus trichotis and Cheirogal
7                                              S-cone ERGs were abnormal in 50% of both groups.
8                                              S-cone ERGs were elicited using adaptation to 650-nm lig
9                                              S-cone terminals, identified by staining for S opsin, sh
10                                              S-cones constitute between 10% and 20% of all cones, the
11                                              S-cones in the cat retina do not form a regular geometri
12 e may be due in part to larger cells with an S cone phenotype in place of rods that failed to differe
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 le L and M cone b-wave activity in ESCS, and S cones may usurp both the space and neural pathways of
17 ontains three classes of cones, the L, M and S cones, which respond preferentially to long-, middle-
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  the relative contribution of melanopsin and S cones, with their overlapping, short-wavelength spectr
21 imilar healthy subjects under achromatic and S-cone isolation conditions.
22 -fold reductions in the mRNAs for M-cone and S-cone opsin, respectively, whereas there was no signifi
23 ity, we studied the effects of luminance and S-cone adaptation on variability in S-cone increment thr
24  a more balanced ratio between luminance and S-cone adaptation than is used for SWAP.
25 nd-site polarization (ratio of luminance and S-cone adaptation; log [Td/Td(S)]).
26 nputs primarily from cones with mixed M- and S-cone pigments.
27                          Responses to M- and S-cone stimuli usually aligned, suggesting that these ce
28 L-cone test but normal performance on M- and S-cone tests.
29                                   On-Off and S-cone ERGs were performed in most adults.
30 rge field of cone pedicles were perused, and S-cone pedicles were identified.
31 explanation based on intrusion from rod- and S-cone-driven responses.
32 he vector, CNGB3 was detected in both M- and S-cones and resulted in increased levels of CNGA3, incre
33 , middle, and short wavelengths (L-, M-, and S-cones) was tested by physiologically and anatomically
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 one mosaic, the spatial relationship between S cones and the first cones to express L/M protein was a
41 low pathway that signals differences between S-cone responses and a sum of L- and M-cone responses; a
42 imetry, possibly due to an imbalance between S-cone adaptation and long (L)- and medium (M)-wavelengt
43 ntly with opsin in both S and L/M cones, but S cones express peripherin and opsin 1 to 3 weeks before
44  and super-normal cone function, mediated by S cones.
45 es, which depend on the SC, can be driven by S-cone input.
46 c inputs differs substantially: in S+ cells, S-cone signals were usually opposed by those of L- and M
47  modulates calcium conductance in the center S cone.
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 -order neurons in the short-wavelength cone (S-cone, blue cone) pedicle and to learn more concerning
51 projections from short-wave-sensitive cones (S cones), and, consistent with this, we found that irrel
52            Short-wavelength-sensitive cones (S-cones) in the retina make little or no contribution to
53 ile comparable losses are not seen in cones, S-cones comprise less than 10% of the cone population, s
54                                 In contrast, S cone density was very low in central retina (0-300/mm(
55                                 In contrast, S-cone pedicles, with more synaptic ribbons, active zone
56  of S cones onto both types could contribute S-cone input for cortical areas primary visual cortex an
57 This results in a delayed, sluggish cortical S-cone signal which is then integrated with L/M-opponent
58 etina have the potential to follow a default S-cone pathway and reveal an essential role for Tr beta
59 and the developmental mechanisms determining S-cone topography are markedly different from the time t
60 NR2E3 in cone precursors and differentiating S-cones of wild-type retina also generated rod-like cell
61 ive +S and -(L+M) receptive fields, and each S cone contributes different weights to different BY gan
62                 Like neighboring cones, each S cone contacts its own OFF midget bipolar cell via tria
63                            However, for each S cone in macaque fovea, there are two S-cone ON bipolar
64                                Overall, each S cone diverges to approximately six BY ganglion cells,
65                          (Specifically, each S cone is presynaptic to four inner S-cone bipolar cells
66                               Moreover, each S-cone OFF midget bipolar cell has a synaptic terminal i
67 one inherited retinal disorder, the enhanced S cone syndrome (ESCS), shows increased visual function,
68                                     Enhanced S-cone syndrome (ESCS) forms part of the differential di
69                                     Enhanced S-cone syndrome (ESCS), featuring an excess number of S
70                                     Enhanced S-cone syndrome has more pleiotropy than previously appr
71 pe of retinal degeneration known as enhanced S-cone syndrome, where patients have a 30-fold increase
72 a in Nrl-knockout mice that exhibit enhanced S-cone function.
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 ced excess M cones in contrast to the excess S cones in Nrl(-/-) mice.
85 l cell-fate determination, leading to excess S cones at the expense of other photoreceptor subtypes.
86 ellular cells and cells receiving excitatory S-cone input but not in parvocellular cells or those rec
87 ity of 10%, with several areas lacking a few S cones that are not coincident with the area of highest
88 as 100% for L and M cone tests and 99.8% for S cones.
89 hought, that the potential image quality for S cones is comparable to that for L and M cones, and tha
90 uning curve and more bandpass, than that for S-cone modulation.
91                                     We found S cone responses only in areas V1 and V2/V3 (peak freque
92          Each foveal S cone diverges to four S-cone ON bipolar cells but contacts them unequally, pro
93                                  Each foveal S cone diverges to four S-cone ON bipolar cells but cont
94 been used to determine the pattern of foveal S cones in both the fetal and adult Macaca and human.
95 ll have a distribution and density of foveal S cones similar to adults, although the high-density rin
96                                       Foveal S-cone increment thresholds were measured on adapting ba
97                      Similarly, signals from S cone-initiated probes were altered by background chang
98 ck exclusively to invaginating contacts from S cones, and in the OFF stratum each cell collects appro
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 d M cones, whereas others receive input from S cones opposed by combined signals from L and M cones.
102 tratified cells, which receive ON input from S cones, fired synchronously with ON parasol and midget
103 ) cells and neurons that received input from S cones.
104 e either excitatory or inhibitory input from S cones.
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 ust bipolar cell dendrites, most likely from S-cone-specific bipolar cells, made synapses at ribbons
108 lue-ON cells receive ON-type excitation from S-cones, and OFF-type excitation from ML-cones.
109 ys: one type receives input exclusively from S-cones, two types receive mixed S/M-cone input and the
110 f neurons that receive excitatory input from S-cones ("S+").
111 f neurons that receive inhibitory input from S-cones ("S-") are quite unlike those of neurons that re
112 orizontal cells received a strong input from S-cones and a weaker input from L- and M-cones.
113 ded from neurons with substantial input from S-cones and found that, on several important dimensions,
114 n individuals lacking L and M cone function (S cone monochromats).
115 ors fated to be rods develop into functional S-cones similar to the human NR2E3 disease.
116 ack M cones and rods, respectively, but gain S cones.
117 paradoxical dilation of the pupil to greater S-cone photon capture.
118                                  The highest S-cone densities are found in three distinct locations:
119                                     However, S-cone responses and light-dependent cGMP hydrolysis wer
120             Although the topography of human S cones is known, the human L- and M-cone submosaics hav
121            All subjects had nearly identical S-cone densities, indicating independence of the develop
122  and their blood supply which likely impacts S-cone function.
123 her weak or silent during photopic vision in S cone monochromats.
124 totransduction proteins are not expressed in S cones until 1 to 3 weeks after the appearance of S ops
125                Lack of both GRK1 and GRK7 in S cones of patients with ESCS results in a more pronounc
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 may result from defective development, known S cone fragility, or abnormal maintenance of mature phot
144  detached cat retina, the density of labeled S-cone outer segments (OS) decreases rapidly as early as
145 entral zone about 100 microm wide that lacks S cones and is surrounded by a ring in which the S-cone
146               Furthermore, neurons with late S-cone inputs exhibit dynamic changes in the sharpness o
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 t contribute to the low sensitivity of mouse S-cones.
154                              The presence of S cone responses and the relative sensitivity of MT neur
155 nctions there have twice the responsivity of S cone contrast-response functions in normal controls.
156 ant lag between their expression and that of S cone opsin indicates that phototransduction proteins a
157                           The convergence of S cones onto both types could contribute S-cone input fo
158 t in the center-surround receptive fields of S cones.
159 ndrome (ESCS), featuring an excess number of S cones, manifests as a progressive retinal degeneration
160                  Estimates of the numbers of S cones missing in the fetal human fovea range from 234
161 tead, showing that they are the terminals of S cones.
162 anges in SC activity depend on the amount of S-cone contrast.
163 e3 is required to suppress the expression of S-cone genes during normal rod differentiation.
164 ral properties, and reflected integration of S-cone inputs via opponent, summing, and intermediate co
165 adaptation conditions with a higher level of S-cone adaptation and/or a more balanced ratio between l
166 s lower for conditions with higher levels of S-cone adaptation (F = 9.04, P = 0.013, for the trained
167  response to rod signals at higher levels of S-cone illumination cannot be eliminated.
168 antly reduced due to a delayed maturation of S-cone to OFF cone bipolar signaling.
169               However, the axon terminals of S-cone photoreceptors were found to express both VGLUT1
170                  We conclude that the use of S-cone stimuli is insufficient to isolate SC function in
171                               Variability of S-cone increment thresholds can be reduced by using adap
172 , lead to loss of rods, increased density of S-cones and supernormal S-cone-mediated vision in humans
173 age is expressed prior to the development of S-cones.
174                   We conclude that excess of S-cones in the rd7 retina originate from photoreceptor p
175 ated with an approximately twofold excess of S-cones.
176  retina thickness and enhanced generation of S-cones, and develop severe early onset retinal dystroph
177 .89 +/- 0.15) because of the fewer number of S-cones in the human retina.
178 These were identified as dendrites of the ON S-cone bipolar cell by immunostaining for the marker cho
179 nputs: an ON bipolar cell that contacts only S-cones and an OFF bipolar cell that contacts L- and M-c
180 patients, who rely on their vision from only S-cones and rods, suffer severely reduced visual acuity
181 rect a common precursor to a rod, M cone, or S cone outcome using Nrl(b2/b2) "knock-in" mice that exp
182  are visible to only one cone type (L, M, or S cone).
183 s of colored letters visible only to L, M or S cones in decreasing steps of cone contrast to determin
184 ence for multiple opsin types within rods or S cones, but immunohistochemistry and partial bleaching
185 toresponses initiated by either rhodopsin or S-cone opsin, and 3) exhibited similar light-activated t
186  express functional Cre-recombinase in M- or S-cones were established in this study.
187 recombinase was functionally active in M- or S-cones.
188  or indeed the magnocellular pathway, as our S-cone stimuli were invisible to this channel also.
189          Adult monkey foveas have an overall S-cone foveal density of 10%, with several areas lacking
190 t- wavelength sensitive cone photoreceptors (S-cones) did not show the adaptive response, and we foun
191 mounts demonstrated the preservation of PNA, S-cone, and rod opsin antibody labeling in the detachmen
192 ow that, in these two trichromatic primates, S-cone distribution and the developmental mechanisms det
193 tor beta lose rods but overproduce primitive S cones that lack outer segments.
194 es to the light signaling pathway to produce S-cone responses.
195                              Second, to pure S-cone modulation, S+ cells are twice as sensitive as S-
196       We found that red-green cells received S-cone input, which aligned with M input, and, unlike bl
197 y TVI curve, but an increase in the relative S-cone illuminance had no effect.
198 fibrillary acidic protein (GFAP), rhodopsin, S-cone opsin, and M/L-cone opsin were performed, as were
199                               However, rods, S-cones, and M-cones activate the ON and OFF circuits vi
200 was tested in a Posner cueing task, the same S-cone stimuli had normal attentional effects, in that t
201  age under photopic achromatic and selective S-cone conditions in peripheral vision and whether any a
202 sible only to the short-wavelength-sensitive S cones interfere with shifts of visual attention but no
203  repression of a short wavelength-sensitive (S) cone differentiation program.
204 d from a blue or short wavelength-sensitive (S) cone On bipolar cell.
205 able analysis of short-wavelength-sensitive (S) cone responses has yet to be achieved and is of consi
206 ave sensitive (M/L) and shortwave sensitive (S) cones in most species, indicating at least dichromati
207 timuli visible only to short-wave-sensitive (S) cones.
208 o stimulation of short wavelength-sensitive (S) cones and decreases to stimulation of middle waveleng
209  of the noise in short wavelength-sensitive (S) cones arose in a later stage of the transduction casc
210 kinetics of ESCS short-wavelength-sensitive (S) cones, when compared with normal L/M cone responses e
211 rs are driven by short-wavelength-sensitive (S) cones.
212  the sparsity of short-wavelength-sensitive (S) cones.
213 he assessment of short-wavelength-sensitive (S)-cone visual function, but has also been shown to have
214  peak sensitivities are at relatively short (S cones), medium (M cones), or long (L cones) wavelength
215 o long (L-cone), middle (M-cone), and short (S-cone) wavelengths.
216 ganglion cells, one is dominated by a single S cone and one is diffusely driven by several.
217               Serial micrographs of a single S-cone pedicle, picked out of the montages, were digitiz
218 agree that the adult human fovea has a small S cone-free area, but data are conflicting concerning S-
219 ive in a therapeutic setting in which strong S-cone transgene expression is required.
220 increased density of S-cones and supernormal S-cone-mediated vision in humans.
221  smaller and briefer dim flash response than S cones.
222 e; L/M cones are more severely affected than S-cones.
223 n of primary visual cortex demonstrated that S cone signals were feedforward in nature and did not ar
224           Critically, however, we found that S cone stimuli did not cause IOR when saccadic eye movem
225  S, L, and M cones in these regions and that S cones may feed into different neural pathways in the c
226        A quantitative analysis suggests that S cones provided about 10% of the input to these cells,
227 hy are markedly different from the time that S cones are first detected.
228 ance signals, leading to the conclusion that S-cone stimuli should be invisible to SC neurons.
229                         The possibility that S-cone stimulation desensitizes the response to rod sign
230                             The premise that S-cone stimuli are invisible to the SC has been used in
231                              We propose that S-cone metabolism is less flexible than in their M/L cou
232 ion of short-wavelength light, suggests that S-cone contributions to this ganglion cell's coextensive
233 lated cone loss in either cone type and that S-cones are as regularly distributed in old as young pri
234                                          The S cone monochromats have clear motion-responsive regions
235 e release onto metabotropic receptors of the S cone bipolar cell dendrite, thereby opening cation cha
236 ow grating down to the spatial cutoff of the S cone mosaic.
237 eady present in the synaptic terminal of the S cone.
238 transduction within the outer segment of the S cone.
239 lls), its spatial density equals that of the S cone; thus it could support psychophysical discriminat
240                                          The S cones in the other species and the M/L cones in all sp
241 sitivity of the pi-1 mechanism driven by the S cones was measured with 440-nm light.
242 t not by background changes seen only by the S cones.
243 es were altered by background changes in the S cones, but not by background changes in the L and M co
244                        The opposition of the S cones is revealed in a seemingly paradoxical dilation
245               In the Microcebus species, the S cones had an inverse topography with very low densitie
246                                          The S-cone and melanopsin photoreceptor channels were found
247                                          The S-cone pedicle arose from a slightly oblique axon and pr
248                                          The S-cone PhNR was the most sensitive test and provided the
249                                          The S-cone terminal thus constitutes the first critical locu
250 ing to a pressure-related mechanism, and the S-cone PhNR was the most sensitive test.
251 nge of lights used in these experiments, the S-cone system apparently does not.
252     Similar functions were generated for the S-cone pathway (isolated using Stiles' two-color thresho
253  being consistent with that expected for the S-cone submosaic.
254 ne-contacting telodendria projected from the S-cone pedicle itself, but a small number of neighboring
255 ic genes while simultaneously inhibiting the S-cone pathway through the activation of Nr2e3.
256 upports the hypothesis that, in mammals, the S-cone lineage was recruited via the Maf-family transcri
257  learn more concerning the uniqueness of the S-cone system in the primate retina.
258 (1.87 +/- 0.08) tests but was reduced on the S-cone test (0.89 +/- 0.15) because of the fewer number
259  Colour discrimination studies show that the S-cone pathway is selectively affected by age and diseas
260                         We conclude that the S-cone pedicle has a unique morphology and connectivity
261 nes and is surrounded by a ring in which the S-cone density is 8%.
262                                        These S-cone terminals are smaller and contain more synaptic r
263                                         This S cone-free zone is detectable at fetal week 15.5 (Fwk15
264 nd the relative sensitivity of MT neurons to S cone and luminance signals agree with functional magne
265                                 Responses to S cone (blue-yellow) and L + M cone (luminance) patterns
266 lar neurons were unequivocally responsive to S cone-isolating stimuli.
267 rrelevant peripheral stimuli visible only to S cones did not produce the saccadic distractor effect p
268                  Extensive diffuse damage to S-cone bipolar and bistratified ganglion cells appears t
269   Fourth, red-green cells often responded to S-cone stimuli.
270 erties of V1 layer 2/3 neurons responsive to S-cone stimulation.
271 ipolar cell provides central elements to two S cones.) These bipolar cells are presynaptic to an equa
272  each S cone in macaque fovea, there are two S-cone ON bipolar cells and two blue-yellow (BY) ganglio
273      While these responses were unequivocal, S cone contrast sensitivity was, on average, 1.0-1.3 log
274 c features of human ESCS, including unstable S-cone-positive photoreceptors.
275 hese results demonstrate that the SC can use S-cone stimuli to guide behavior.
276        The assumption that the SC cannot use S-cone stimuli to guide behavior has never been tested.
277 nd M cones centrally and feed into the usual S cone pathways.
278 L, and second, if NRL fails to act, M versus S cone identity dictated by TRbeta2.
279 cone opsin and suppressing short-wavelength (S) cone opsin.
280  medium-wavelength (M) and short-wavelength (S) cone opsins.
281 increased approximately 2-fold, and 92% were S cones.
282 ith tiny spots in the central foveola, where S cones, and thus S opponent (S(o)) cell activity, are l
283     L/M cones were regularly spaced, whereas S cones showed no regular distribution pattern.
284                         To determine whether S cones contact ON and OFF midget bipolar cells as well
285               Early human NR2E3 disease with S cone hyperfunction showed thickened retinal layers wit
286 wfully modulated in contrast, and occur with S-cone stimuli invisible to the retinotectal route.
287 ient of cone distribution is disturbed, with S-cones becoming widespread across the retina.
288 ], red-green [(L - M)-cone] and blue-yellow (S-cone) modulations at various temporal frequencies.
289                                In this zone, S cones were 9-14% of all cones.

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