ライフサイエンスコーパス: ocular dominance

1 epresentations (for example, orientation and ocular dominance).

2 ceral organ asymmetry, brain laterality, and ocular dominance.

3 Eyes were randomized by ocular dominance.

4 ands which lack any periodic alternations in ocular dominance.

5 vation (MD), facilitated cortical changes in ocular dominance.

6 ce does not affect the overall expression of ocular dominance.

7 sion of deprived-eye responses or a shift in ocular dominance after brief monocular deprivation.

8 Here we show that local circuits for ocular dominance always have smooth and graded transitio

9 The role of age, sex, ocular dominance, amount of monovision, and hyperopic ve

10 When the local maps for ocular dominance and binocular disparity both had measur

11 However, the precise local arrangement of ocular dominance and binocular disparity maps provide ne

12 udies that examined the relationship between ocular dominance and binocular disparity of individual c

13 ening and closing of the critical period for ocular dominance and how changes in cortical responsiven

14 Together with a shift in ocular dominance and large effects on unit activity duri

15 features of topographic organization such as ocular dominance and orientation columns in primary visu

16 They are necessary for formation of ocular dominance and orientation columns in visual corte

17 that allows us to analyze it in relation to ocular dominance and orientation patterns.

18 Brief monocular deprivation (MD) shifts ocular dominance and reduces the density of thalamic syn

19 mulus dimensions including spatial location, ocular dominance and stimulus orientation.

20 being more myopic are related to laterality, ocular dominance, and magnitude of anisometropia.

21 tivity for orientation, direction of motion, ocular dominance, and other properties of first-order (l

22 e continuous representations of orientation, ocular dominance, and retinotopy that, to fit in two dim

23 anisotropy is reflected in the orientation, ocular dominance, and spatial frequency domains, which a

24 reasons that remain unclear, the patterns of ocular dominance are very diverse across species and can

25 The maps for spatial location and ocular dominance arise from the spatial arrangement of t

26 These results thus reveal ocular dominance as a key driver of the binocular matchi

27 ormal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject

28 ayers and of geniculocortical afferents into ocular dominance bands.

29 sion, monocular deprivation (MD) also shifts ocular dominance by potentiation of open-eye responses.

30 ovided conflicting results regarding whether ocular dominance can predict the selectivity or sensitiv

31 the spiking activity of individual neurons, ocular dominance cannot predict binocular disparity tuni

32 , H-ras(G12V) not only increased the rate of ocular dominance change in response to monocular depriva

33 The classic model of ocular dominance column development, in which spontaneou

34 consistent with this model but suggest that ocular dominance column formation begins between P7 and

35 ore the critical period there is a period of ocular dominance column formation during which there is

36 tant questions about whether activity guides ocular dominance column formation in this 'precritical p

37 vation also suggests that the mechanisms for ocular dominance column formation may be partially disti

38 tivity-dependent plasticity, we propose that ocular dominance column formation relies on the targetin

39 ening and maintaining active synapses during ocular dominance column formation.

40 y indicated that norepinephrine (NE) permits ocular dominance column plasticity during the critical p

41 ivity-based competition is believed to drive ocular dominance columns (ODC) in mammals and in experim

42 lasticity of the blob system and that of the ocular dominance columns (ODC) varied with the degree of

43 The mechanisms that give rise to ocular dominance columns (ODCs) during development are c

44 Ocular dominance columns (ODCs) have been well studied i

45 ctional enucleation of one eye to reveal the ocular dominance columns (ODCs) of the primary visual co

46 tracortical excitatory input to deprived-eye ocular dominance columns (ODCs) relative to nondeprived-

47 llosal cells with the underlying patterns of ocular dominance columns (ODCs) revealed transneuronally

48 Ocular dominance columns (ODCs), and blob vs. interblob

49 ns rats is a consequence of the existence of ocular dominance columns (ODCs), and of callosal patches

50 ous retinal activity in the establishment of ocular dominance columns and synaptic refinement at reti

51 tions were most obvious in monkeys with fine ocular dominance columns and were invisible in monkeys w

52 However, the border strips at the edges of ocular dominance columns appeared pale, reflecting a los

53 nal hypothesis proposed by Hubel and Wiesel, ocular dominance columns are already substantially forme

54 otrophins in the formation and plasticity of ocular dominance columns as well as in the regulation of

55 ons interact; iso-orientation contours cross ocular dominance columns at right angles, and ocular dom

56 The emergence of ocular dominance columns before the onset of the critica

57 on, consistent with recent observations that ocular dominance columns can be detected at these early

58 Thus, the organization of ocular dominance columns cannot fully account for the pa

59 cular dominance columns at right angles, and ocular dominance columns distort retinotopy near the V1/

60 When subplate neurons are ablated, ocular dominance columns do not form in the visual corte

61 rrelated spontaneous activity and functional ocular dominance columns during early ferret postnatal d

62 the geniculocortical projection showed that ocular dominance columns emerge by 3 weeks of age in cat

63 s to the emergence of layers, retinotopy, or ocular dominance columns for the selective connectivity

64 ithin the vestibular nucleus, resembling the ocular dominance columns formed in three-eyed frogs.

65 patches in the upper layers were centered on ocular dominance columns in layer 4C, with one exception

66 hanges in the horizontal connections between ocular dominance columns in the upper layers, which reor

67 ion and CO activity were reduced in deprived ocular dominance columns of the visual cortex and in dep

68 Thalamocortical axons segregate into ocular dominance columns several weeks before the onset

69 The pattern then reorganizes into ocular dominance columns that are roughly equally distri

70 is region, metabolic activity was reduced in ocular dominance columns that normally would be driven b

71 Ocular dominance columns were present in all cases, havi

72 No ocular dominance columns were visible in opercular corte

73 ctivity was reduced in the ipsilateral eye's ocular dominance columns which serve peripheral temporal

74 ropriate eye-specific laminae in the LGN and ocular dominance columns within primary visual cortex.

75 mical representation of the two eyes, called ocular dominance columns, in primary visual cortex.

76 In the classic model for the development of ocular dominance columns, initially overlapping geniculo

77 ast three overlapping local modular systems: ocular dominance columns, orientation pinwheels, and cyt

78 e alternating pale and dark bands resembling ocular dominance columns.

79 oline was injected into one eye to label the ocular dominance columns.

80 ive fields and to enable connections for the ocular dominance columns.

81 ion selective responses and the formation of ocular dominance columns.

82 rned via anatomical characteristics, as with ocular dominance columns.

83 began at age 4 months, causing shrinkage of ocular dominance columns.

84 ye was conspicuous as an oval region without ocular dominance columns.

85 es characterized by an absence of pronounced ocular dominance columns.

86 gregation of geniculocortical afferents into ocular dominance columns.

87 niculocortical axons during the formation of ocular dominance columns.

88 ominated, OFF-centric and runs orthogonal to ocular dominance columns.

89 New approaches to the study of ocular dominance development, a model system for the dev

90 Unlike orientation selectivity and ocular dominance, direction selectivity was not detected

91 ic cats, we observed a dramatic shift in the ocular dominance distribution of simple cells, the first

92 he development of axonal connections between ocular dominance domains and compartments within macaque

93 The ocular dominance imbalance away from the affected eye wa

94 The decrease in ocular dominance imbalance in V2 was the neuronal change

95 find a relationship between speed tuning and ocular dominance in all three areas that MD preferential

96 Changes of ocular dominance in the visual cortex can be induced by

97 Monocular deprivation normally alters ocular dominance in the visual cortex only during a post

98 In controls, MD results in a shift of the ocular dominance index (ODI) from a baseline of 0.15 to

99 The shift in ocular dominance induced by brief monocular deprivation

100 Plasticity extends to visual features beyond ocular dominance, involving subcortical and cortical reg

101 The anatomy that underlies retinotopy and ocular dominance is well known, but no anatomical struct

102 no LGNd is arranged into hemiretinal and not ocular dominance laminae.

103 Monocular deprivation during the CP affects ocular dominance, limits visual performance, and contrib

104 We removed the ocular dominance map by monocular enucleation in newborn

105 us position (retinotopic map) and eye input (ocular dominance map) that results from the precise arra

106 e use these measurements to demonstrate that ocular dominance maps follow a common organizing princip

107 between these possibilities, we measured the ocular dominance (OD) and disparity selectivity of neuro

108 tion [MD]) during the critical period alters ocular dominance (OD) by shifting the responsiveness of

109 an essential role of subplate neurons during ocular dominance (OD) column formation in the developing

110 s in tangential sections were related to the ocular dominance (OD) column structure as deduced from c

111 s illustrated by mapping patterns similar to ocular dominance (OD) columns within superficial and dee

112 ntralateral to the NDE during MD and shifted ocular dominance (OD) in favor of the NDE in both hemisp

113 ritical period can yield enduring changes to ocular dominance (OD) in primary visual cortex (V1).

114 Brief monocular deprivation (MD) shifts ocular dominance (OD) in primary visual cortex by causin

115 Maps of orientation preference (OP) and ocular dominance (OD) in the primary visual cortex of fe

116 rons classified as monocular by conventional ocular dominance (OD) measurements.

117 (MD) during the critical period (CP) shifts ocular dominance (OD) of cortical responsiveness toward

118 The ocular dominance (OD) of individual cortical neurons var

119 closure (MC) causes a profound shift in the ocular dominance (OD) of neurons in primary visual corte

120 As demonstrated by optical imaging, rapid ocular dominance (OD) plasticity after brief monocular d

121 rivation (MD) engages synaptic mechanisms of ocular dominance (OD) plasticity and generates robust in

122 ole of GluA1 in the homeostatic component of ocular dominance (OD) plasticity has not so far been tes

123 We addressed this question by studying ocular dominance (OD) plasticity in mice that were stimu

124 Ocular dominance (OD) plasticity in mouse primary visual

125 Ocular dominance (OD) plasticity in the mouse primary vi

126 Ocular dominance (OD) plasticity in the visual cortex is

127 recording method to document the kinetics of ocular dominance (OD) plasticity induced by temporary li

128 2 of the 50+ MHCI genes H2-K(b) and H2-D(b), ocular dominance (OD) plasticity is enhanced.

129 of primary visual cortex (V1) in adult mice: ocular dominance (OD) plasticity resulting from monocula

130 ated recently an important role for sleep in ocular dominance (OD) plasticity, a classic form of in v

131 exposure leads to a persistent disruption in ocular dominance (OD) plasticity.

132 normal critical period of activity-dependent ocular dominance (OD) plasticity.

133 ion of inhibition and for the proper sign of ocular dominance (OD) plasticity.

134 avor of the nondeprived eye, a process named ocular dominance (OD) plasticity.

135 erience-dependent cortical plasticity is the ocular dominance (OD) shift in visual cortex after monoc

136 The ocular dominance (OD) shift that occurs in visual cortex

137 Ocular dominance (OD) shifts in favor of open-eye stimul

138 Monocular deprivation (MD) induces ocular dominance (OD) shifts through biphasic changes in

139 the critical period, Arc induction reflects ocular dominance (OD) shifts within the binocular zone.

140 e two eyes during the critical period shifts ocular dominance (OD) towards the more active eye.

141 t of visual features, including orientation, ocular dominance (OD), and spatial frequency (SF), whose

142 uli through each eye, which determines their ocular dominance (OD).

143 erm occlusion of either eye markedly changes ocular dominance (OD).

144 t from one eye or the other, which is termed ocular dominance (OD).

145 ion (< or =3 d) induces a rapid shift in the ocular dominance of binocular neurons in the juvenile ro

146 n to predict the orientation selectivity and ocular dominance of neighboring neurons.

147 Importantly, the ocular dominance of neurons in thalamo-recipient laminae

148 as much more rapid and severe effects on the ocular dominance of neurons in the primary visual cortex

149 deprivation also failed to elicit a shift in ocular dominance or open-eye potentiation.

150 Activation resembling ocular dominance or orientation columns has been mapped

151 ture maps representing the cortical neurons' ocular dominance, orientation and direction preferences

152 functional maps of visual properties (e.g., ocular dominance, orientation preference, and spatial-fr

153 ties into multiple maps such as retinotopic, ocular dominance, orientation preference, direction of m

154 bour' periodicities for the hypercolumns for ocular dominance, orientation, colour and disparity, and

155 ions of visual cortex containing alternating ocular dominance patches, periodic fluctuations in corre

156 anatomic correlate of this early functional ocular dominance pattern.

157 Here we show that the formation of ocular dominance patterns follows a common organizing pr

158 a new image-processing algorithm to measure ocular dominance patterns more accurately than in the pa

159 In this model, the different ocular dominance patterns simply emerge from differences

160 n, and regulation of the critical period for ocular dominance plasticity (Hanover et al., 1999; Huang

161 +)) interneurons, can induce a new period of ocular dominance plasticity (ODP) after the endogenous p

162 We show that such models cannot reproduce ocular dominance plasticity (ODP) because negative feedb

163 Ocular dominance plasticity (ODP) following monocular de

164 ind that Ts65Dn mice demonstrate a defect in ocular dominance plasticity (ODP) following monocular de

165 ary for the onset of the critical period for ocular dominance plasticity (ODP) in the postnatal visua

166 and long-term depression (LTD) in vitro and ocular dominance plasticity (ODP) in vivo.

167 we tested the role of CREB, SRF, and MEF2 in ocular dominance plasticity (ODP), a paradigm of activit

168 lular events involved in this process during ocular dominance plasticity (ODP)-a canonical form of in

169 nsiveness to that eye, a phenomenon known as ocular dominance plasticity (ODP).

170 od (pre-CP) and the critical period (CP) for ocular dominance plasticity (ODP).

171 ed critical period [a process referred to as ocular dominance plasticity (ODP)].

172 ere then monocularly deprived at the peak of ocular dominance plasticity after a prolonged alcohol-fr

173 Ocular dominance plasticity after brief (24 hours) monoc

174 ransplantation of inhibitory neurons induces ocular dominance plasticity after the critical period.

175 1 knockout animals retain juvenile levels of ocular dominance plasticity and their visual acuity rema

176 GABAergic inhibition is necessary to trigger ocular dominance plasticity and to modulate the onset an

177 We propose that adult ocular dominance plasticity arises from compensatory mec

178 during a brief period of development impairs ocular dominance plasticity at a later age.

179 t, differences in inhibitory innervation and ocular dominance plasticity between NF1 mice and WT litt

180 l neurons terminates the critical period for ocular dominance plasticity but also indicate that, in g

181 phorylation is required for the induction of ocular dominance plasticity but is not needed for its st

182 report that persistent, rapid, juvenile-like ocular dominance plasticity can be reactivated in adult

183 r regulates activity-dependent mechanisms of ocular dominance plasticity during cortical development.

184 n particular, is thought to be essential for ocular dominance plasticity during monocular deprivation

185 tatory synapses onto FS INs, which inhibited ocular dominance plasticity during the critical period b

186 SPn removal also alters ocular dominance plasticity during the critical period.

187 ing eliminates monocular deprivation-induced ocular dominance plasticity during the normal cortical c

188 prevents the physiological effects of MD on ocular dominance plasticity examined in vivo.

189 geniculate nucleus (dLGN) can undergo rapid ocular dominance plasticity following monocular deprivat

190 on in adulthood and thus to limit functional ocular dominance plasticity in adult primary visual cort

191 ivation through dark exposure restores rapid ocular dominance plasticity in adult rats.

192 rom the medial ganglionic eminence reinstate ocular dominance plasticity in adult recipients.

193 on facilitated dendritic spine reduction and ocular dominance plasticity in adult visual cortex.

194 s neuregulin via inhibition of erbBs rescued ocular dominance plasticity in adults, allowing recovery

195 e a reduction in inhibition is necessary for ocular dominance plasticity in both juvenile and adult a

196 To test this hypothesis, we assessed ocular dominance plasticity in genetically engineered mi

197 vivo inhibition of miR-132 in mice prevented ocular dominance plasticity in identified neurons follow

198 o fast spiking interneurons, which inhibited ocular dominance plasticity in juveniles but rescued pla

199 adulthood can, like the critical period for ocular dominance plasticity in mammals, be extended by b

200 insights may force a revision in how data on ocular dominance plasticity in mutant mice have been int

201 s neuregulin via inhibition of erbBs rescued ocular dominance plasticity in postcritical period adult

202 For the best-studied case, ocular dominance plasticity in primary visual cortex in

203 nous nicotinic signaling modulator, enhances ocular dominance plasticity in the adult primary visual

204 We found that reactivation of ocular dominance plasticity in the adult visual cortex i

205 Ocular dominance plasticity in the developing primary vi

206 inpocetine, a PDE type I inhibitor, restores ocular dominance plasticity in the ferret model of fetal

207 Ocular dominance plasticity in the primary visual cortex

208 l studies have addressed this question using ocular dominance plasticity in the visual cortex as a mo

209 vern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice

210 -term potentiation induction and by impaired ocular dominance plasticity in the visual cortex.

211 re initiated in adulthood reactivates robust ocular dominance plasticity in the visual cortex.

212 well as mice that express APPswe alone, lack ocular dominance plasticity in visual cortex.

213 ively regulates the homeostatic component of ocular dominance plasticity in visual cortex.

214 Furthermore, Ube3a-deficient mice lacked ocular dominance plasticity in vivo when challenged with

215 nts in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo.

216 The enhanced ocular dominance plasticity induced by visual deprivatio

217 Ocular dominance plasticity is a well-documented phenome

218 Ocular dominance plasticity is a widely studied model of

219 Ocular dominance plasticity is easily observed during th

220 These findings suggest that ocular dominance plasticity is regulated by the executio

221 ortical development, the critical period for ocular dominance plasticity is shortened in NF1 mice due

222 s suggest that structural changes underlying ocular dominance plasticity occur rapidly following mono

223 could be a permissive factor regulating the ocular dominance plasticity of the developing cortex.

224 mically, the molecular mechanisms underlying ocular dominance plasticity remain unknown.

225 igate differences between adult and juvenile ocular dominance plasticity using Fourier optical imagin

226 orientation tuning was degraded and onset of ocular dominance plasticity was delayed and remained ope

227 Here, we show that initiation of ocular dominance plasticity was impaired with reduced CS

228 Additionally, silent synapse-based ocular dominance plasticity was largely independent of t

229 was provided by the finding that blockade of ocular dominance plasticity was reversible; animals trea

230 le; animals treated with HSV-mCREB recovered ocular dominance plasticity when mCREB expression declin

231 ogy revealed that alcohol exposure disrupted ocular dominance plasticity while preserving robust visu

232 mice is hyperexcitable and unable to express ocular dominance plasticity, although many aspects of vi

233 r the termination of the critical period for ocular dominance plasticity, and can rescue deficits ind

234 FS interneurons play an instructive role in ocular dominance plasticity, causing disinhibition among

235 Ocular dominance plasticity, classically thought to be r

236 ry synaptic transmission or facilitate rapid ocular dominance plasticity, demonstrating the presence

237 tarting at a later age (P20) did not disrupt ocular dominance plasticity, indicating that timing of e

238 Since the discovery of ocular dominance plasticity, neuroscientists have unders

239 classic form of cortical plasticity in vivo (ocular dominance plasticity, ODP; [8, 9]) in the cat vis

240 After induction of ocular dominance plasticity, the stability of the induce

241 d in adult mice past the critical period for ocular dominance plasticity, which is reported to end at

242 geniculate, protein synthesis impaired rapid ocular dominance plasticity, while leaving neuronal resp

243 ral role in enabling the critical period for ocular dominance plasticity.

244 lopmental model of systems-level plasticity, ocular dominance plasticity.

245 on of neuronal responses, a process known as ocular dominance plasticity.

246 visual deprivation from birth, like that of ocular dominance plasticity.

247 reexpression of iLTD and the reactivation of ocular dominance plasticity.

248 g a restricted postnatal critical period for ocular dominance plasticity.

249 nd in turn influences the critical period of ocular dominance plasticity.

250 synaptic transmission, and earlier onset of ocular dominance plasticity.

251 the maturation of GABAergic innervation and ocular dominance plasticity.

252 ion of GABAergic inhibition and the onset of ocular dominance plasticity.

253 enable the persistent reactivation of rapid ocular dominance plasticity.

254 e Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity.

255 period of monocular deprivation will induce ocular dominance plasticity.

256 vidence that calcineurin is also involved in ocular dominance plasticity.

257 vivo to permit structural remodeling during ocular dominance plasticity.

258 onstrate that CREB function is essential for ocular dominance plasticity.

259 ble to autophosphorylate show impairments in ocular dominance plasticity.

260 investigated a role for protein synthesis in ocular dominance plasticity.

261 In this article, we present a theory of ocular dominance plasticity.

262 rol of the timing of the critical period for ocular dominance plasticity.

263 duced PV cell activity allows for excitatory ocular dominance plasticity.

264 demonstrate that microglia are critical for ocular dominance plasticity.

265 ponse to monocular deprivation and abrogates ocular dominance plasticity.

266 ses, resulting in reopening of juvenile-like ocular dominance plasticity.

267 itical periods resulted in lifelong juvenile ocular dominance plasticity.

268 er than an instructive role of inhibition in ocular dominance plasticity.

269 utant mice lacking functional PirB, cortical ocular-dominance plasticity is more robust at all ages.

270 he changes occurred irrespective of regional ocular dominance preference and were independently media

271 Ocular dominance probably has a significant impact on He

272 othesis that the developmental plasticity of ocular dominance reflects competitive interactions for s

273 oss species that aligns the cortical axis of ocular dominance segregation with the axis of slowest re

274 We used these estimates to calculate ocular dominance separately for excitation and suppressi

275 inocular competition and demonstrate that an ocular dominance shift can occur solely by the mechanism

276 ase using HSV injections did not prevent the ocular dominance shift during monocular deprivation.

277 by and thin spine density and enhancement of ocular dominance shift in adult V1 of Lynx1 knock-out (K

278 ic inhibition of tPA activity can ablate the ocular dominance shift in Lynx1 KO mice.

279 ad to complete dominance by the open eye, an ocular dominance shift.

280 ty during the critical period as assessed by ocular dominance shifts in response to monocular depriva

281 Ocular dominance shifts in visually deprived adults are

282 possible explanation for the variability in ocular dominance shifts observed in individual neurons a

283 otein kinase A (PKA) by Rp-8-Cl-cAMPS blocks ocular dominance shifts that occur following monocular d

284 and might be one of the mechanisms promoting ocular dominance shifts.

285 work, two ingredients are crucial to observe ocular dominance shifts: a sufficient level of inhibitio

286 elation between local axes of distortion and ocular dominance slabs, which they intersect at angles o

287 strong correlation between eccentricity and ocular dominance stripe width.

288 i segregates along an axis orthogonal to the ocular dominance stripes, as recently demonstrated in ca

289 s, such as in the development of patterns of ocular dominance stripes.

290 owest retinotopic gradient orthogonal to the ocular dominance stripes.

291 red at rest, modulates the susceptibility of ocular dominance to deprivation [6-10].

292 One eye of each patient was randomized by ocular dominance to flap creation with a femtosecond las

293 lar cortical neurons used monocular tests of ocular dominance to infer binocular function.

294 The sensitivity of ocular dominance to regulation by monocular deprivation

295 ed matched orientation tuning preference and ocular dominance to the principal neuron.

296 ice exhibited normal visual acuity, baseline ocular dominance was abnormal and resembled that observe

297 Ocular dominance was determined by hole-in-the-card test

298 At the level of single cells, ocular dominance was unrelated to binocular disparity se

299 responsive to the deprived eye, and maps of ocular dominance were no longer evident using intrinsic-

300 pical dendrites, as well as firing rates and ocular dominance, were normal.