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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 neurons receiving opposing inputs from L and M cones.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 (1.84 +/- 0.08 log contrast sensitivity) and M-cone (1.87 +/- 0.08) tests but was reduced on the S-co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 .8- and 2.6-fold reductions in the mRNAs for M-cone and S-cone opsin, respectively, whereas there was

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

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

84 50% of the IPL receive inputs primarily from M-cones, and the HBC(M/SC)s with axon terminals ramifyin

85 ediating preferential expression of Pias3 in M cones.

86 verexpression and M-opsin underexpression in M cones.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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