ライフサイエンスコーパス: M-cone

1 Gtf2ird1-null mice also demonstrate abnormal M cone and rod electrophysiological responses.

2 Attempting to activate M cones exclusively is shown to elicit a color beyond th

3 e cone spectral sensitivities and activating M cone cells exclusively.

4 Additionally, M-cone dark adaptation was largely suppressed in CRALBP-

5 eniculate nucleus (LGN) in mice with altered M-cone spectral sensitivity (Opn1mw(R)) and multispectra

6 l role for Tr beta 2 in the commitment to an M-cone identity.

7 contrast thresholds for drifting L cone and M cone gratings summed in different spatial phases.

8 he periphery, however, there is little L and M cone b-wave activity in ESCS, and S cones may usurp bo

9 otion responses in individuals lacking L and M cone function (S cone monochromats).

10 unds and H1 horizontal cells get mixed L and M cone input, likely indiscriminately sampled from the r

11 uenced responses with the same sign as L and M cone inputs (i.e., no color opponency).

12 al H1 and ganglion cells inherit their L and M cone inputs from the photoreceptor mosaic unmodified b

13 eedback from horizontal cells that sum L and M cone inputs linearly and without selectivity, complete

14 The relative strength of L and M cone inputs to H1 and ganglion cells at the same locat

15 We measured the relative strengths of L and M cone inputs to H1 horizontal cells and parasol and mid

16 If so, the segregation of L and M cone inputs to receptive field centers and surrounds w

17 strictly random rule for assigning the L and M cone photopigments.

18 d receptive field structure to combine L and M cone signals antagonistically and thereby establish a

19 L and M cone synaptic inhibition is feedforward and thus occur

20 rming normal color vision was 100% for L and M cone tests and 99.8% for S cones.

21 excitatory-type synaptic contacts with L and M cone types in humans, but not in macaques or marmosets

22 tion of S-OFF midget cells combine S, L, and M cone inputs along noncardinal directions of color spac

23 re observed, including decrease in the S and M cone function and lack of rod photoreceptor function.

24 nt, multi-site phosphorylation of both S and M cone opsins by in situ phosphorylation and isoelectric

25 er mouse cone arrestin (mCAR) or mouse S and M cone opsins revealed specific binding of mCAR to light

26 staining with antibodies to rod opsin, S and M cone opsins, cytochrome oxidase, synaptophysin, glial

27 nt-cell types, either differencing the L and M cones (L(o) and M(o) cells), or the S vs. L + M cones

28 L and M cones also had higher dark apo-opsin noise than holo-p

29 d-green pathway, in which signals from L and M cones are opposed, is associated with the specialized

30 lanopsin signals add with signals from L and M cones but are opposed by signals from S cones in contr

31 in ESCS, S cones may partially replace L and M cones centrally and feed into the usual S cone pathway

32 erally received synergistic input from L and M cones in both the center and the surround.

33 establish functional connections with L and M cones indiscriminately, implying that the cone-selecti

34 t signals from probes initiated in the L and M cones were affected by backgrounds that changed the me

35 ting backgrounds, the sensitivities of L and M cones were, on average, receptor-type specific, but in

36 for S cones is comparable to that for L and M cones, and that macular pigment has no significant fun

37 anged the mean absorption rates in the L and M cones, but not by background changes seen only by the

38 that receives subtractive inputs from L and M cones, either L-M or M-L.SIGNIFICANCE STATEMENT This a

39 s generate slower light responses than L and M cones, show much smaller changes in response kinetics

40 had highly disordered arrangements of L and M cones, three subjects showed evidence for departures f

41 e neurons receive opponent inputs from L and M cones, whereas others receive input from S cones oppos

42 levels increase, and are noisier than L and M cones.

43 , but not by background changes in the L and M cones.

44 ation from S cones and inhibition from L and M cones.

45 s that receive nonselective input from L and M cones.

46 cones opposed by combined signals from L and M cones.

47 neurons receiving opposing inputs from L and M cones.

48 l cells that are driven by surrounding L and M cones.

49 which receive ON input primarily from L and M cones.

50 signals originating in S cones versus L and M cones; notably, S-cone signals appear perceptually del

51 ere are different distributions of S, L, and M cones in these regions and that S cones may feed into

52 ized by complete loss (of) or reduced L- and M- cone function due to defects in the OPN1LW/OPN1MW gen

53 d absolute sensitivities of the UV-cone- and M-cone-driven b-wave responses of C57BL/6 mice.

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

55 cells, rescued the retinal visual cycle and M-cone sensitivity in knockout mice.

56 ormal subjects were sensitive to both L- and M-cone modulations.

57 racterized by functional loss of both L- and M-cone opsins due to mutations in the OPN1LW/OPN1MW gene

58 nse to stimuli bleaching up to 99% of L- and M-cone opsins were measured with high resolution, phase-

59 al electron micrographs, we show that L- and M-cone pedicles in macaque fovea are presynaptic to appr

60 The L- and M-cone PhNRs may have a role in monitoring established g

61 minance pathway that signals a sum of L- and M-cone responses.

62 hway that signals differences between L- and M-cone responses; a blue-yellow pathway that signals dif

63 between S-cone responses and a sum of L- and M-cone responses; and a luminance pathway that signals a

64 pear perceptually delayed relative to L- and M-cone signals.

65 a band-pass response of the pupil to L- and M-cone signals.

66 of human S cones is known, the human L- and M-cone submosaics have resisted analysis.

67 re obtained from all subjects to both L- and M-cone-isolating modulations and to intermediate modulat

68 ield mapping argues for segregation of L-and M-cone signals to the midget cell center and surround, b

69 the OFF pathway originated with both rod and M-cone signaling.

70 nglion cells in these retinas combine S- and M-cone inputs antagonistically, but no direct evidence l

71 ntly modulate synaptic sensitivity of S- and M-cone networks.

72 The retinal gradient in S- and M-cone opsin (co-)expression has traditionally been cons

73 lating excitation of the native mouse S- and M-cone opsin classes.

74 , echoing the topographic gradient in S- and M-cone opsin expression.

75 osition, which governs the balance of S- and M-cone opsin input due to the opsin expression gradient

76 S- and M-cone OS showed a gradual recovery in length after reat

77 (1.84 +/- 0.08 log contrast sensitivity) and M-cone (1.87 +/- 0.08) tests but was reduced on the S-co

78 However, rods, S-cones, and M-cones activate the ON and OFF circuits via distinct pa

79 For most observers, signals from L- and M-cones combine linearly.

80 ulations were chosen to stimulate the L- and M-cones in various ratios.

81 length sensitive cone photoreceptors (L- and M-cones) from adapting.

82 cells, smooth cells summed input from L- and M-cones, lacked measurable S-cone input, showed high spi

83 zontal cells received input only from L- and M-cones, whereas H2 horizontal cells received a strong i

84 ifferences in the relative numbers of L- and M-cones.

85 function of the contrasts seen by the L- and M-cones.

86 and an OFF bipolar cell that contacts L- and M-cones.

87 from S-cones and a weaker input from L- and M-cones.

88 nals were usually opposed by those of L- and M-cones; in S- cells, signals from L-cones were usually

89 yer (IPL) receive mixed inputs from rods and M-cones, the HBC(MC)s with axon terminals ramifying betw

90 er by direct synaptic contacts from rods and M-cones.

91 Degeneration rates of S- and M-cones are negatively correlated with expression levels

92 Moreover, the visual function of S- and M-cones is markedly preserved in the KI;Fatp4 (-/-) mice

93 Bipolar cells that sum signals from S- and M-cones may signal to ganglion cells that encode luminan

94 re and function with equal effects on S- and M-cones.

95 ones were usually opposed to those of S- and M-cones.

96 ation was not affected by the lack of AWAT2, M-cone dark adaptation both in isolated retina and in vi

97 bright red) and by a stimulus that decreased M-cone activity (appearing dark red).

98 Samd7 represses S-opsin expression in dorsal M-cones-analogous to its role in repressing UV cone gene

99 mparison indicates that the signal from each M cone makes a larger contribution to the ERG than each

100 (b2/b2) mice lacked rods and produced excess M cones in contrast to the excess S cones in Nrl(-/-) mi

101 inding may represent a general mechanism for M cone degeneration in multiple forms of cone degenerati

102 retina, however, the threshold intensity for M-cone-driven responses was two log units greater than t

103 .8- and 2.6-fold reductions in the mRNAs for M-cone and S-cone opsin, respectively, whereas there was

104 ng TRbeta2 transcription factor required for M-cone differentiation) and S-opsin and may, therefore,

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

106 50% of the IPL receive inputs primarily from M-cones, and the HBC(M/SC)s with axon terminals ramifyin

107 ened photopic b-wave implicit time, improved M-cone visual function, and substantially deaccelerated

108 ated proteasome stress plays a major role in M cone degeneration in Lrat(-/-) model.

109 s in darkness, being ~30% in L cones, ~3% in M cones, and negligible in S cones.

110 ediating preferential expression of Pias3 in M cones.

111 verexpression and M-opsin underexpression in M cones.

112 Responses to S cone (blue-yellow) and L + M cone (luminance) patterns were measured in area V1 and

113 Ds) that combine L/M cone-opponent and S/L + M cone-opponent signals following the rules predicted fr

114 lled the red-green pathway, and an S vs. L + M cone circuit linked to the small bistratified ganglion

115 ones (L(o) and M(o) cells), or the S vs. L + M cones (S(o) cells), relatively few striate cortex simp

116 The intrinsic, rod and (L + M) cone-derived light responses combine in these giant c

117 targeted the L + M + S, L - M, and S - (L + M) cone combinations.

118 functions were measured for luminance [(L + M)-cone], red-green [(L - M)-cone] and blue-yellow (S-co

119 or luminance [(L + M)-cone], red-green [(L - M)-cone] and blue-yellow (S-cone) modulations at various

120 PhNRs from the L&M-cone pathways were elicited by a 200-msec pulse of red

121 at 550 nm, suggesting strong initial S and L+M cone contribution.

122 Blue-yellow (S versus L+M cone) opponency is mediated by a growing family of low

123 and combined long- and medium-wavelength (L+M) cone functions were also fit and compared.

124 om 445 nm (all three functions) to 487 nm (L+M-cone and melanopsin functions only), suggesting signif

125 on the L-M axis could be well explained by L-M cone contrast and did not show a clear red bias when L

126 fer between red and green stimuli of equal L-M cone contrast.

127 signals arising from the recently evolved L-M cone system, not the older S-cone channel.

128 ast and did not show a clear red bias when L-M cone contrast was properly equalized.

129 ional characteristics of the tarsier S and L/M cone systems are yet to be determined, tarsier cone pr

130 , full-length scRNA-seq revealed that both L/M cone and rod precursors co-expressed NRL and THRB RNAs

131 nt functional domains (COFDs) that combine L/M cone-opponent and S/L + M cone-opponent signals follow

132 Moreover, early L/M cone precursors sequentially expressed several lncRNAs

133 Only 15% of the cones expressed L/M cone opsin, and some coexpressed S cone opsin.

134 itive (S) cones, when compared with normal L/M cone responses evoked by the same stimulus, were slowe

135 PDE, and RK are expressed together in the L/M cone OS shortly after L/M opsin appears.

136 Q, we documented an abnormal ratio of S to L/M cone function and progressive retinal degeneration.

137 L/M cones appear outside the central retina by Fwk 21.5 an

138 L/M cones were regularly spaced, whereas S cones showed no

139 (2) the spatial relationship between S and L/M cones at the time of initial opsin expression, and (3)

140 of phototransduction proteins within S and L/M cones suggests that some local signal(s) coordinates t

141 ars concomitantly with opsin in both S and L/M cones, but S cones express peripherin and opsin 1 to 3

142 on abnormally and then rapidly degenerate; L/M cones are more severely affected than S-cones.

143 Normal deactivation kinetics in human L/M cones can occur without GRK7 when GRK1 is present in E

144 and opsin 1 to 3 weeks before neighboring L/M cones.

145 with ESCS were similar to those of normal L/M cones.

146 vated much more slowly than ESCS or normal L/M cones.

147 Some S+L/M cones are still detected in adult retina.

148 nti-long/medium wavelength-sensitive (anti-L/M) cone opsin or anti-glial fibrillary acidic protein (G

149 etics of long/middle-wavelength-sensitive (L/M) cone-mediated responses in patients with ESCS were si

150 with MYCN, which composed the seventh most L/M-cone-specific regulon, and SYK, which was implicated i

151 F receptive field are larger than opponent L/M-cone contributions via outer diffuse bipolar cells and

152 er diffuse bipolar cells and that opponent L/M-cone signals are conveyed mainly by inner S-cone bipol

153 The altered ratio of S- to L/M-cone photoreceptor sensitivity in ESCS may be due to a

154 slocalization, lack CNGB3 labelling in the L/M-cones, and lack GC1 in all cones.

155 L:M cone ratio estimates were correlated highly with those

156 In a third retina, the L:M cone ratio differed significantly at two retinal locat

157 ural retina leucine zipper factor (NRL) lack M cones and rods, respectively, but gain S cones.

158 ntaining protein 1 (GTF2IRD1) in maintaining M cone cell identity and function as well as rod functio

159 s are at relatively short (S cones), medium (M cones), or long (L cones) wavelengths.

160 aximally sensitive to long (L-cone), middle (M-cone), and short (S-cone) wavelengths.

161 pigment) and a second near 510 nm [midwave (M)-cone pigment].

162 ng CRALBP exhibited M-opsin mislocalization, M-cone loss, and impaired cone-driven visual behavior an

163 sary for restricting its expression to mouse M cones or that such elements are not recognized in mous

164 he contrast detection threshold of the mouse M-cones and rods.

165 adult RDH8/ABCA4-deficient mice have normal M-cone morphology but reduced visual acuity and photores

166 ansducin y and resulted in partial rescue of M-cone-mediated light responses.

167 cone viability, corrected mis-trafficking of M-cone opsin and restored cone PDE6 expression.

168 and ABCA4 suppressed the dark adaptation of M-cones driven by both the intraretinal visual cycle and

169 hotoreceptors and RPE for dark adaptation of M-cones.

170 ta 2) in mice, causing the selective loss of M-cones and a concomitant increase in S-opsin immunoreac

171 etina is established by the preponderance of M-cones that constitute between 80% and 90% of all cones

172 naptic conductances evoked by selective L or M cone stimulation in the midget ganglion cell dendritic

173 dominant excitatory input from a single L or M cone.

174 X-chromosome inactivation would favor L- or M-cone clumping, there was no evidence of clumping, perh

175 onency and cannot contribute selective L- or M-cone input to the midget cell surround.

176 r2e3 enhances rhodopsin, but represses S- or M-cone opsin transcription when interacting with Crx.

177 Bipolar cells that carry S- or M-cone signals can have a role in color discrimination a

178 he proteasome stress and completely prevents M cone degeneration in Lrat(-/-)Opn1sw(-/-) mice (a pure

179 RA signaling early was sufficient to promote M cone fate and suppress L cone fate in retinal organoid

180 Our data suggest that RA promotes M cone fate early in development to generate the pattern

181 eration in Lrat(-/-)Opn1sw(-/-) mice (a pure M cone LCA model, Opn1sw encoding S-opsin) for at least

182 d the remaining types receive an almost pure M-cone signal.

183 nt M-opsin delivered by AAV5 vectors rescues M-cone function in Opn1mw (-/-) mice.

184 e RPE in Mct8-deficient mice partly restores M cone identity, consistent with paracrine-like control

185 We further found that in the dorsal retina, M-cones and melanopsin contribute to dark-adapted DAC re

186 TRbeta2 direct a common precursor to a rod, M cone, or S cone outcome using Nrl(b2/b2) "knock-in" mi

187 by rods under dim lighting conditions, rods/M-cones/melanopsin under intermediate lighting condition

188 Fast (f) and slow (s) M-cone input signals of the same polarity (+sM and +fM)

189 vely from S-cones, two types receive mixed S/M-cone input and the remaining types receive an almost p

190 -sensitive (S) versus medium-wave-sensitive (M) cone identity, and maintain their nature and function

191 tebrate rod and medium wavelength-sensitive (M) cone photoreceptors differentiate by repression of a

192 nsitive (L) and medium-wavelength-sensitive (M) cones, rods, and melanopsin.

193 nsitive (S) and middle-wavelength-sensitive (M) cones.

194 nsitive (S) and middle-wavelength-sensitive (M) cones.

195 itution between 450 nm and 535 nm to silence M-cone response at luminances higher than rod saturation

196 At these less intense levels, fast and slow M-cone signals of opposite polarity (-sM and +fM) cancel

197 t rod signals in retinal regions with sparse M-cone opsin expression.(10-13) The relative importance

198 early human eye development, suggesting that M cones are generated before L cones.

199 required for a half-maximum response, of the M-cone population was 38-fold lower than that of the rod

200 ecreased contrast sensitivity limited to the M-cone test.

201 Though M-cone density decreases smoothly to the ora serrata whe

202 olor vision that varied in the ratio of L to M cones (from 1.1:1 to 16.5:1).

203 The proportion of L to M cones is strikingly different in two male subjects, ea

204 eptors does not attenuate or modify L versus M cone antagonism, discounting both presynaptic and post

205 thout recourse to any inner retinal L versus M cone inhibitory pathways.

206 n cell dendritic tree and show that L versus M cone opponency arises presynaptic to the midget cell a

207 iated largely by the segregation of L versus M cone signals to the centre versus the surround of the

208 Red-green (L versus M cone) opponency appears to be mediated largely by the

209 cting evidence for either random or L versus M cone-selective inhibitory circuits has divergent impli

210 nent pathways are well established: an L vs. M cone circuit linked to the midget ganglion cell type,

211 M', from the long-wave (L) and middle-wave (M) cones.

212 ing in mice by activating medium-wavelength (M) cone opsin and suppressing short-wavelength (S) cone