ライフサイエンスコーパス: ocular dominance

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

2 ands which lack any periodic alternations in ocular dominance.

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

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

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

6 Eyes were randomized by 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 Together with a shift in ocular dominance and large effects on unit activity duri

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

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

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

17 ocked, cortical cells fail to develop normal ocular dominance and orientation selectivity.

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

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

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

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

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

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

26 ad increased considerably but the pattern of ocular dominance bands did not yet appear mature.

27 The pattern and degree of modulation of the ocular dominance bands resembled that in adult animals b

28 30 ferret kits, no modulation reminiscent of ocular dominance bands was detectable in the pattern of

29 The development of ocular dominance bands was studied by transneuronal labe

30 ayers and of geniculocortical afferents into ocular dominance bands.

31 o eyes in the region rostral to the periodic ocular dominance bands.

32 able ferret are segregated into eye-specific ocular dominance bands.

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

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

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

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

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

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

39 k-rearing throughout the critical period for ocular dominance column formation decreases levels of BD

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

41 -containing subplate neurons are involved in ocular dominance column formation in the ferret visual s

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

43 Ocular dominance column formation in visual cortex depen

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

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

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

47 visual cortex during the critical period for ocular dominance column formation.

48 levels by the end of the critical period for ocular dominance column formation.

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

50 ct LGN tracer injections revealed segregated ocular dominance columns <7 days after innervation of la

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

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

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

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

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

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

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

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

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

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

61 in the same region of visual cortex in which ocular dominance columns are absent.

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

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

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

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

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

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

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

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

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

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

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

73 Ocular dominance columns form in ferrets between postnat

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

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

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

77 es in the LGN coincident with development of ocular dominance columns in the visual cortex.

78 The initial establishment of ocular dominance columns in visual cortex is believed to

79 lateral geniculate nucleus (LGN) axons into ocular dominance columns is believed to involve a prolon

80 al fibers cross at the optic chiasm, and (2) ocular dominance columns normally found in cortex are re

81 CO columns usually fit in register with the ocular dominance columns of the fixating eye, suggesting

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

83 ssed either for autoradiography to label the ocular dominance columns or for cytochrome oxidase (CO)

84 neous activity, we propose that formation of ocular dominance columns relies on molecular cues presen

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

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

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

88 Ocular dominance columns were present in all cases, havi

89 No ocular dominance columns were visible in opercular corte

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

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

92 P14 to P56 fails to prevent the formation of ocular dominance columns, although NOS activity is reduc

93 ble decrease in CaMKII-beta mRNA in deprived ocular dominance columns, especially of layer IVCbeta.

94 ressive reduction of NRF-2 alpha in deprived ocular dominance columns, in parallel with decreases in

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

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

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

98 ation, CO revealed a low-contrast pattern of ocular dominance columns, resembling the pattern in monk

99 in layer IVc, corresponding precisely to the ocular dominance columns, whereas eyelid suture produced

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

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

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

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

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

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

106 gregation of geniculocortical afferents into ocular dominance columns.

107 niculocortical axons during the formation of ocular dominance columns.

108 modeling known to accompany the formation of ocular dominance columns.

109 tex alters the development and plasticity of ocular dominance columns.

110 ernating stripes with periodicity normal for ocular dominance columns.

111 esponded to the core zones of the open eye's ocular dominance columns.

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

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

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

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

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

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

118 In ferret, however, ocular dominance domains in different regions of the vis

119 inputs form a nearly uniform array of small ocular dominance domains, while preserving overall topog

120 The ocular dominance imbalance away from the affected eye wa

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

122 Cortical maps for orientation and ocular dominance in the primary visual cortex of cats we

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

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

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

126 The shift in ocular dominance induced by brief monocular deprivation

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

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

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

130 ent of ocularly matched orientation maps and ocular dominance maps can be achieved either simultaneou

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Ocular dominance (OD) plasticity in mouse primary visual

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

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

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

149 2 of the 50+ MHCI genes H2-K(b) and H2-D(b), ocular dominance (OD) plasticity is enhanced.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 Activation resembling ocular dominance or orientation columns has been mapped

168 rea 17 but revealed no finer organization of ocular dominance or orientation selectivity.

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

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

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

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

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

174 o clustering consistent with the presence of ocular dominance patches.

175 anatomic correlate of this early functional ocular dominance pattern.

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

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

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

179 Ocular dominance plasticity (ODP) following monocular de

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

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

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

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

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

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

186 Ocular dominance plasticity after brief (24 hours) monoc

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

188 1 knockout animals retain juvenile levels of ocular dominance plasticity and their visual acuity rema

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Ocular dominance plasticity in the developing primary vi

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

213 Ocular dominance plasticity in the primary visual cortex

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

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

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

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

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

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

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

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

222 The enhanced ocular dominance plasticity induced by visual deprivatio

223 Ocular dominance plasticity is a widely studied model of

224 Ocular dominance plasticity is easily observed during th

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

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

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

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

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

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

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

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

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

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

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

236 mGluR2/3 changes with the critical period of ocular dominance plasticity, a form of sensory-dependent

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

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

239 Ocular dominance plasticity, classically thought to be r

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

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

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

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

244 e RIbeta isoform of PKA is not essential for ocular dominance plasticity, which can proceed despite d

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

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

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

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

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

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

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

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

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

254 the maturation of GABAergic innervation and ocular dominance plasticity.

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

256 enable the persistent reactivation of rapid ocular dominance plasticity.

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

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

259 period of monocular deprivation will induce ocular dominance plasticity.

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

261 vivo to permit structural remodeling during ocular dominance plasticity.

262 demonstrate that microglia are critical for ocular dominance plasticity.

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

264 ble to autophosphorylate show impairments in ocular dominance plasticity.

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

266 ponse to monocular deprivation and abrogates ocular dominance plasticity.

267 pressed in mouse visual cortex did not block ocular dominance plasticity.

268 rlier termination of the critical period for ocular dominance plasticity.

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

270 itical periods resulted in lifelong juvenile ocular dominance plasticity.

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

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

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

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

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

276 Ocular dominance probably has a significant impact on He

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

278 The development of ocular dominance requires that the correlations of an in

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

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

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

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

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

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

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

286 Ocular dominance shifts in visually deprived adults are

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

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

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

290 ry for segregation of retinal afferents into ocular dominance stripes in the doubly innervated tadpol

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

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

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

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

295 The sensitivity of ocular dominance to regulation by monocular deprivation

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

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

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

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

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