ライフサイエンスコーパス: deprived eye

1 ausing neurons to lose responsiveness to the deprived eye.

2 ual geniculocortical arbors representing the deprived eye.

3 little or no overall loss of response to the deprived eye.

4 to subsequent visual stimulation through the deprived eye.

5 ps seen in the hemisphere ipsilateral to the deprived eye.

6 n the A laminae that received input from the deprived eye.

7 nable significant functional recovery of the deprived eye.

8 e than it reduced background activity in the deprived eye.

9 of responsiveness of cortical neurons to the deprived eye.

10 vealed a profound shift in favour of the non-deprived eye.

11 y complete loss of visual responses from the deprived eye.

12 o the monocular segment contralateral to the deprived eye.

13 ex by causing depression of responses to the deprived eye.

14 delayed strengthening of inputs from the non-deprived eye.

15 effect on the hemisphere ipsilateral to the deprived eye.

16 ls continued to respond more strongly to the deprived eye.

17 markedly decreased visual acuity through the deprived eye.

18 of cortical responses to stimulation of the deprived eye.

19 e hemisphere contralateral to the previously deprived eye.

20 ed for the loss of cortical responses to the deprived eye.

21 ation prevented the loss of responses to the deprived eye.

22 eous recovery of responses to the previously deprived eye.

23 in cortical responses to stimulation of the deprived eye.

24 layers of visual cortex dominated by the non-deprived eye.

25 s respond poorly to stimuli presented to the deprived eye.

26 a matching anatomical loss of input from the deprived eye.

27 roduced little or no loss of response to the deprived eye.

28 over rates were similar for control and form-deprived eyes.

29 scleral regions was measured in control and deprived eyes.

30 there was difference between the normal and deprived eyes.

31 ed in differentially expressed genes in form-deprived eyes.

32 ith the altered retinal biochemistry in form-deprived eyes.

33 P = 0.027) in the posterior scleras of form-deprived eyes.

34 ads to a rapid depression of inputs from the deprived eye and a delayed strengthening of inputs from

35 n produces increased axial elongation of the deprived eye and a myopic shift in refractive state.

36 o a loss of responsiveness of neurons to the deprived eye and a shift in response toward the open eye

37 l cortex rapidly lose their responses to the deprived eye and ultimately lose many of their inputs fr

38 activity within the fibrous scleras of form-deprived eyes and paired contralateral recovering eyes w

39 5, cortical cells remained responsive to the deprived eye, and maps of ocular dominance were no longe

40 uction of feedforward input representing the deprived eye, and that an unexpected weakening of cortic

41 lity, first decreasing responsiveness to the deprived eye, and then slowly increasing responsiveness

42 n which synapse number is reduced by half in deprived-eye arbors.

43 Responses were measured for the normal and deprived eyes at a variety of contrasts, and curves fitt

44 and physiology of the visual cortex, and the deprived eye becomes amblyopic.

45 fter P100 did not reduce the response to the deprived eye below that to the nondeprived eye.

46 ion prevented loss of responses to the newly deprived eye but did not prevent simultaneous recovery o

47 ved-eye patches responded only weakly to the deprived eye but were well tuned for the same stimulus o

48 urons cease to respond to stimulation of the deprived eye, but how this occurs is poorly understood.

49 Deprived-eye collagen mRNA levels were lower than contro

50 brous scleras of experimentally myopic (form-deprived) eyes, control eyes, and eyes recovering from f

51 t visual cortex suggest that, in addition to deprived-eye depression, monocular deprivation (MD) also

52 Synapses that are eliminated in deprived eye domains have low basal CaMKII activity, imp

53 synapses of layer 2/3 pyramidal cells within deprived eye domains, despite reduced visual drive, but

54 ng monocular stimulation correlated with the deprived eye dominance.

55 ed that mediate the loss of responses to the deprived eye during monocular deprivation.

56 The small number of neurons dominated by the deprived eye exhibited poor tuning characteristics.

57 monocular deprivation (MD), the shrinkage of deprived-eye geniculocortical arbors is less than half-m

58 branches and loss of presynaptic sites from deprived-eye geniculocortical arbors.

59 ent with the hypothesis that a rapid loss of deprived-eye geniculocortical presynaptic sites is respo

60 can maintain functional connections with the deprived eye (i.e., reducing undersampling for the affec

61 ponsiveness to stimulation of the originally deprived eye in most cortical cells could be restored by

62 uction of cortical regions responsive to the deprived eye in normal animals, but not in ferrets expos

63 This shift was achieved by a decline in deprived-eye input that was saturated within 2 d and did

64 d exhibit precocious potentiation of the non-deprived eye inputs.

65 on of NMDA receptors in the pathway from the deprived eye, like the reduction of acetylcholine recept

66 Compared with the control eyes, deprived-eye MMP-2 mRNA levels were higher and MMP-3 lev

67 fate incorporation by chondrocytes from form-deprived eyes more effectively than those from normal ey

68 al-cortex-dependent behavior through the non-deprived eye (NDE) during deprivation, and enabled enhan

69 ecrease in intracortical excitatory input to deprived-eye ocular dominance columns (ODCs) relative to

70 inhibitory presynaptic sites in layer IV of deprived-eye ODCs relative to nondeprived columns.

71 However, if the deprived eye of a monocularly deprived kitten is simply

72 nd scleral chondrocytes from normal and form-deprived eyes of 10- to 14-day-old chicks were treated w

73 At the onset of unrestricted vision, the deprived eyes of 18 of the diffuser-reared monkeys and 1

74 ed monkeys were more hyperopic than the form-deprived eyes of the normal-light-reared monkeys.

75 ion of gelatinase A was increased by 128% in deprived eyes (P = 0.009), whereas after 1 day of recove

76 Neurons in regions surrounding the deprived-eye patches responded only weakly to the depriv

77 These deprived-eye patches were located on the pinwheel center

78 The coincidence of deprived-eye patches with pinwheel center singularities,

79 ective loss of orientation tuning within the deprived-eye patches, indicate that the orientation and

80 It has been thought that the deprived-eye pathway will fail to compete against the op

81 ecrease in GABA strongly correlated with the deprived eye perceptual boost measured by binocular riva

82 ual but incomplete recovery of acuity in the deprived eye preceded by a loss of the enhanced acuity i

83 ession of the response to stimulation of the deprived eye, previously only reported in juveniles, and

84 e rate of vitreous chamber elongation in the deprived eye (r2 = 0.779, P < or = 0.05).

85 cluding loss of visual responsiveness to the deprived eye, reduced visual acuity, and loss of tuning

86 es ocular balance, unexpectedly boosting the deprived eye, reflecting homeostatic plasticity [11, 12]

87 ntly reduced in the posterior sclera of form-deprived eyes relative to total collagen content (-36.19

88 ved-eye response without a change in the non-deprived eye response, NR2A-knockout mice fail to exhibi

89 We find that MI fails to induce deprived-eye response depression but promotes potentiati

90 normally causes a profound depression of the deprived-eye response without a change in the non-depriv

91 als and single-unit recordings revealed that deprived eye responses and orientation selectivity recov

92 Moreover, recovery of deprived eye responses was not dependent upon mRNA trans

93 hanges, which were largely driven by loss of deprived eye responses, were tightly regulated with stru

94 s essential for loss but not for recovery of deprived eye responses.

95 etely blocked the OD shift and depression of deprived-eye responses after MD without affecting baseli

96 istinct, noncompetitive processes, a loss of deprived-eye responses followed by an apparently homeost

97 causes a significantly greater depression of deprived-eye responses in kitten visual cortex than does

98 of the RW mice was mediated by a decrease of deprived-eye responses in V1, a signature of "juvenile-l

99 eeks of binocular exposure, some recovery of deprived-eye responses occurred when chondroitinase had

100 Arc(-/-) mice did not exhibit depression of deprived-eye responses or a shift in ocular dominance af

101 TNFalpha reveals the normal initial loss of deprived-eye responses, but the subsequent increase in r

102 Deprived-eye responsiveness was lost in the extragranula

103 ed in a significant degree of myopia in form-deprived eyes resulting from significant lengthening of

104 lar visual deprivation actually improves the deprived eye's competitive advantage during a subsequent

105 asticity, in which neurons innervated by the deprived eye show a remarkable capacity to compensate fo

106 veness of primary visual cortical neurons to deprived eye stimulation, and morphological plasticity,

107 rons had already lost their responses to the deprived eye, subsequent NT-4/5 infusion could restore t

108 eral ocular tissues in both control and form-deprived eyes suggests that melatonin, acting through sp

109 s and the synthesis rates of decorin in form-deprived eyes suggests that proteoglycan synthesis withi

110 ly shorter within the posterior pole of form-deprived eyes (t1/2 = 7.212 days) compared with the same

111 and MMP-2 mRNA levels were 66% higher in the deprived eyes than in the control eyes.

112 tical period (CP) reduces the ability of the deprived eye to activate cortex, but the underlying cell

113 r in addition), the decreased ability of the deprived eye to activate cortical neurons could be due t

114 Deprived-eye VEPs were no larger in the injected hemisph

115 NRG1 treatment prevents the loss of deprived eye visual cortical responsiveness in vivo.

116 a 4 d MD with a reduction in its response to deprived eye visual stimulation, the transgenic mouse V1

117 Alternatively, deprived-eye visual responses could be suppressed by an

118 Therefore, the rapid loss of deprived-eye visual responsiveness following MD is due n

119 The rapid loss of responsiveness to deprived-eye visual stimulation could be due to a decrea

120 eduction in visual cortex area driven by the deprived eye was much less pronounced in ethanol-treated

121 Interestingly, when the deprived eye was opened in adults, there was a gradual b

122 When the deprived eye was re-opened during the critical period, c

123 A contribution to background activity in the deprived eye was reduced compared to the NMDA contributi

124 The deprived eye was reopened, the functional architecture o

125 x, and both these features reversed when the deprived eye was reopened.

126 oration by chondrocytes from normal and form-deprived eyes was inhibited by mAChR antagonists with a

127 B activation in recovery of responses to the deprived eye, we used herpes simplex virus (HSV) to expr

128 ts towards the open eye and weakening of the deprived eye were seen in layer 4 after the critical per

129 Maps of intrinsic optical responses from the deprived eye were weaker and less well tuned for orienta

130 Ocular dimensions of normal and deprived eyes were examined by high frequency A-scan ult

131 tropias, and in 6 of these monkeys, the form-deprived eyes were more hyperopic than their fellow eyes

132 n of excitation and inhibition driven by the deprived eye, while reducing the inhibition but preservi