ライフサイエンスコーパス: chiasm

1 m the ventrotemporal retina toward the optic chiasm.

2 ther cross or avoid the midline at the optic chiasm.

3 nifestation of disorders involving the optic chiasm.

4 tended ectopically-dorsal and lateral to the chiasm.

5 ther cross or avoid the midline at the optic chiasm.

6 isolated from cortex, optic nerve and optic chiasm.

7 ons results in robust RGC axon exit from the chiasm.

8 retinal axon growth in the developing optic chiasm.

9 y making axonal guidance errors at the optic chiasm.

10 ells with uncrossed projections at the optic chiasm.

11 ic brain during formation of the mouse optic chiasm.

12 l groups that lie within the nerve and optic chiasm.

13 they remain grouped in the lateral nerve and chiasm.

14 tgrowth, including path-finding at the optic chiasm.

15 sure, which is located adjacent to the optic chiasm.

16 tory tract, mammillothalamic tract, or optic chiasm.

17 ic haemangiopericytoma compressing the optic chiasm.

18 and hypoplasia of the optic nerve and optic chiasm.

19 divergence associated with the albino optic chiasm.

20 after birth (P24) at the centre of the optic chiasm.

21 They disappeared in the chiasm.

22 ntly facilitate retinal axon crossing in the chiasm.

23 d for efficient RGC decussation at the optic chiasm.

24 ding of the ganglion cell axons at the optic chiasm.

25 tely affects axonal growth through the optic chiasm.

26 factor expressed in nasal retina and at the chiasm.

27 ssorting of RGC axons as they exit the optic chiasm.

28 additional axonal exclusion zones within the chiasm.

29 ogenesis and axonal growth through the optic chiasm.

30 isorders affecting the optic nerve and optic chiasm.

31 nd anomalous axonal pathfinding at the optic chiasm.

32 planes 1-mm thick and parallel to the optic chiasm.

33 f high Hs2st and/or Hs6st1 expression at the chiasm.

34 f HSPG sulfation in RGC axon guidance at the chiasm.

35 embryos display axon disorganization at the chiasm.

36 he RGCs themselves, most likely at the optic chiasm.

37 ill project axons to the brain via the optic chiasm.

38 in the developing Foxg1-/- retina and optic chiasm.

39 Foxg1 is also expressed at the optic chiasm.

40 ralateral targets, thereby forming the optic chiasm.

41 encephalon during the formation of the optic chiasm.

42 ut mice and analyzed their retinas and optic chiasms.

43 n to cross or avoid the midline at the optic chiasm, a critical guidance maneuver that establishes th

44 Thus, within the optic chiasm, a sequence of positional transformations occur t

45 na and in the region of the developing optic chiasm, a ventral midline structure in which retinal gan

46 f heparan sulfation on RGCs and at the optic chiasm and (2) this differential sulfation directs retin

47 Chiasm defects include axon stalling in the chiasm and a reduction in the total number of RGCs proje

48 ted with reference to disorders of the optic chiasm and anophthalmia (absence of the eyes).

49 cular locations in the retina and around the chiasm and are normally deployed to prevent axons enteri

50 axons exhibited normal crossing at the optic chiasm and fasciculation of the optic nerve.

51 uidance factors, and the absence of an optic chiasm and forebrain commissures.

52 predetermined crossing pattern in the optic chiasm and grew to the ipsilateral LGN.

53 es, such as pathfinding of RGCs at the optic chiasm and hippocampal long-term potentiation and long-t

54 fibers affects the organization of the optic chiasm and lateral geniculate nuclei (LGN) in human albi

55 e optic nerves, chiasm and tracts, and optic chiasm and LGN volume compared with controls (P < 0.001

56 tly control RGC axon divergence at the optic chiasm and may additionally function as a general inhibi

57 ->and markedly reduced the size of the optic chiasm and optic nerves.

58 reduced axonal midline crossing at the optic chiasm and optic tract fasciculation.

59 Between E30 and E35, the optic chiasm and optic tract remain acellular, but the latter

60 The optic chiasm and splenium of the corpus callosum were transect

61 etinal order when the axons pass through the chiasm and that this order is maintained throughout the

62 It is dorsally bounded by the optic chiasm and the alar hypothalamus, and caudally by the di

63 We have examined the optic chiasm and the retina in albino and normally pigmented w

64 l and contralateral projections at the optic chiasm and the subsequent segregation of retinal inputs

65 Axon organization in the optic chiasm and tract and RGC growth cone morphologies are al

66 antly smaller diameters of the optic nerves, chiasm and tracts, and optic chiasm and LGN volume compa

67 body of the optic stalk and nerve, the optic chiasm and ventral diencephalon, and the anterior midlin

68 y of the optic nerve (1.5 mm anterior to the chiasm) and retina showed no injury 1 week after Mn(2+)

69 d temporal retinal fibers cross at the optic chiasm, and (2) ocular dominance columns normally found

70 approximately half of these axons cross the chiasm, and a rare subset ( approximately 1%) manages to

71 of the ciliary body, retina, optic nerve and chiasm, and central visual pathways.

72 h electrodes implanted on the cornea, in the chiasm, and on the cortex.

73 Whole mounts of optic nerve, chiasm, and optic tract were sectioned horizontally and

74 ght microscopic analysis of the optic nerve, chiasm, and optic tracts of Rana pipiens after the anter

75 identical tracing of the optic nerve, optic chiasm, and optic tracts to the level of the lateral gen

76 talk, cross the ventral midline at the optic chiasm, and terminate in the optic tectum of the zebrafi

77 cord, the hindbrain and midbrain, the optic chiasm, and the median eminence in the forebrain.

78 equentially through the prechiasmatic nerve, chiasm, and tract.

79 le brain, oriented so that the optic nerves, chiasm, and tracts were in the same plane.

80 In addition, responsiveness of optic nerve-, chiasm- and cortex-derived O-2A/OPCs to thyroid hormone

81 ignificant numbers and fail to form an optic chiasm; and (4) axons in multiple commissural tracts of

82 mechanisms for axon divergence in the optic chiasm are discussed in the context of other popular mod

83 s, in the tree shrew, optic fascicles in the chiasm are often separated by thick collagen bundles.

84 ar and subventricular zones and in the optic chiasm, areas that are rich in oligodendrocyte (OL) prog

85 ns leave the chiasm at the same level of the chiasm as do their contralateral counterparts.

86 Ipsilateral axons leave the chiasm at the same level of the chiasm as do their contr

87 termining the relative position of the optic chiasm at the ventral midline of the developing hypothal

88 sulfation directs retinal axons through the chiasm, at least in part by modulating the response of t

89 In the ipsilateral chiasm, axons diverge to form three central, optic tract

90 At the optic chiasm, axons from either eye meet and decide whether to

91 crete layers of the medulla and in the outer chiasm between the lamina and medulla.

92 s of axonal staining progressed to the optic chiasm by 7 days and remained undetectable at 2 weeks.

93 sted whether the albino mutation affects the chiasm by studying 'chimeric' cultures of retinal explan

94 e 2), to reflect its similarity to irregular chiasm C-roughest and Kirrel.

95 roteins, including Drosophila RST (irregular chiasm C-roughest) protein and mammalian KIRREL (kin of

96 otein and mammalian KIRREL (kin of irregular chiasm C-roughest), NEPH1, and NPHS1 (nephrin) proteins.

97 on in vitro rescues the inhibitory effect of chiasm cells and eliminates the ipsilateral projection i

98 projection and reduces neurite outgrowth on chiasm cells in an age- and region-specific manner.

99 RGCs, contralateral RGC axons grow poorly on chiasm cells in vitro and project ipsilaterally at the c

100 'chimeric' cultures of retinal explants and chiasm cells isolated from pigmented and albino mice.

101 m Foxd1 deficient retina are not repulsed by chiasm cells, and in vivo many VT RGCs aberrantly projec

102 wth when grown on either pigmented or albino chiasm cells, demonstrating that the albino mutation doe

103 through actions in nasal retina, and that in chiasm cells, Foxg1 is required for the generation of a

104 ressing with Foxg1-null retinal explants and chiasm cells, we provide functional evidence that Foxg1

105 In retina-chiasm co-cultures, VT RGCs from Foxd1 deficient retina

106 of periods of advance was more brief in the chiasm compared to those in the optic nerve and tract.

107 nt of diseases of the orbit, optic nerve and chiasm continue to evolve.

108 d in directing axon growth in the developing chiasm, correlate with the expression patterns of severa

109 P-43-deficient axons are cultured with optic chiasm, cortical, or dorsal midbrain cells.

110 Chiasm defects include axon stalling in the chiasm and a

111 in the pattern of decussation at their optic chiasm, demonstrating that a melanin-related agent is cr

112 s within 2 days, oligodendrocytes arose from chiasm-derived cells after 5 days and from cortical O-2A

113 nglion cell (RGC) axons at the midline optic chiasm determines whether RGCs project to ipsilateral or

114 but in double mutant mice a large additional chiasm developed anterior to the true chiasm, many retin

115 n factor known for its role in eye and optic chiasm development, causes the rostral oral ectoderm to

116 Here, we review recent findings on optic chiasm development, highlighting the specific transcript

117 by which axons chose their route through the chiasm during development will have to be expanded.

118 Electrical stimulation of the optic chiasm elicits reduced calcium transients and impaired v

119 cross the diencephalon midline at the optic chiasm en route to their brain targets.

120 ptic chiasm, we cocultured mouse retinal and chiasm explants in collagen gels.

121 he ventral surface of the brain at the optic chiasm for sorting into the optic tracts.

122 e Eph family of receptor tyrosine kinases in chiasm formation.

123 on growth and/or reorganization during optic chiasm formation.

124 de guidance information for RGC axons during chiasm formation.

125 ssion in the ventral diencephalon influences chiasm formation.

126 s in other midline decisions), but where the chiasm forms.

127 in the ventral diencephalon where the optic chiasm forms.

128 ent from the ventral midline where the optic chiasm forms.

129 eloping ventral diencephalon where the optic chiasm forms.

130 dline, thus forming the bodily crossed optic chiasm found in fish.

131 asm itself) or extrinsic (compression of the chiasm from an adjacent structure).

132 Optic nerve from EAE and optic chiasm from MS also showed decreased cholesterol synthes

133 mice) in which mice develop optic nerve and chiasm glioma.

134 Consequently, in the chiasm, growth cones spent relatively more time pausing

135 The albino mutation acts at the chiasm in a similar manner in both groups even though th

136 ns and the cellular composition of the optic chiasm in albino mice are similar to those of normally p

137 Within the chiasm, individual contralaterally projecting axons grow

138 s localized to the floor plate and the optic chiasm, intermediate targets located at the ventral midl

139 rtion of the optic nerve at the level of the chiasm into the contralateral optic tract.

140 nglion cell (RGC) axon growth from the optic chiasm into the optic tract are unknown.

141 ons fail to progress normally from the optic chiasm into the optic tracts.

142 Chiasm involvement and severe vision deterioration occur

143 The mouse optic chiasm is a model for axon guidance at the midline and f

144 The optic chiasm is an important choice point at which retinal gan

145 how that this delayed RGC axon exit from the chiasm is characterized by abnormal randomized axon rout

146 Interestingly, expression in the optic chiasm is high at postnatal day 6, but decreases with th

147 In affected animals, the optic chiasm is missing, and each retina projects entirely to

148 categorized as intrinsic (thickening of the chiasm itself) or extrinsic (compression of the chiasm f

149 ve named this gene Kirrel2 (kin of irregular chiasm-like 2), to reflect its similarity to irregular c

150 tional chiasm developed anterior to the true chiasm, many retinal axons projected into the contralate

151 plex of Sema6D, Nr-CAM, and Plexin-A1 at the chiasm midline alters the sign of Sema6D and signals Nr-

152 VEGF164 is expressed at the chiasm midline and is required for normal contralateral

153 a permissive midline signal for axons at the chiasm midline and provide in vivo evidence that VEGF-A

154 Ephrin-B2 is expressed at the mouse chiasm midline as the ipsilateral projection is generate

155 ls in vitro and project ipsilaterally at the chiasm midline in vivo, and Plexin-A1 and Nr-CAM express

156 ne for the progression of RGC axons from the chiasm midline into the contralateral optic tract.

157 e nucleus (dLGN), when crossing at the optic chiasm midline is altered.

158 Unusual RGC axon trajectories include chiasm midline recrossing similar to abnormal CNS midlin

159 away from its ligand, ephrinB2, at the optic chiasm midline, and a transcription factor Zic2, that, l

160 RGC) axons from nasal retina cross the optic chiasm midline, whereas temporal retina axons do not and

161 late RGC axon repulsion by cues at the optic chiasm midline.

162 ects the ipsilateral projection at the optic chiasm, misrouted RGCs target the appropriate retinotopi

163 lacking Foxd1, both retinal development and chiasm morphogenesis are disrupted.

164 associated with axonal behavior at the optic chiasm must affect ganglion cells in a cell-extrinsic ma

165 ssed on midline radial glia and Plexin-A1 on chiasm neurons, and Plexin-A1 and Nr-CAM are also expres

166 diencephalic preoptic area, where the optic chiasm normally forms.

167 racts and in the corpus callosum (CC), optic chiasm (Och), and internal capsule.

168 However, the present study shows that the chiasm of a highly visual eutherian mammal, the tree shr

169 Here we have found that the enlarged chiasm of GAP-43 null mouse embryos appears subsequent t

170 In the optic chiasm of mammals, axons either cross the midline to the

171 The optic chiasm of marsupials differs from that of the eutherian

172 -/-) mice but missing were entirely in optic chiasms of Brn3b/Brn3c double knockout mice, suggesting

173 l axons cross the neuraxis to form the optic chiasm on the hypothalamus in a position defined by over

174 oth in determining the position of the optic chiasm on the ventral diencephalon (presumptive hypothal

175 ect axons along the optic nerve to the optic chiasm on the ventral surface of the hypothalamus.

176 ll proteins is similar, occupying the entire chiasm, optic tracts, and prechiasmatic portion of the o

177 The core is located above the optic chiasm, receives primary and secondary visual afferents,

178 The chiasm reduced retinal neurite lengths and numbers, but

179 Here, we show that ephrin-Bs in the chiasm region direct the divergence of retinal axons thr

180 isms that mediate axon exit from the midline chiasm region or defects in growth cone signaling requir

181 Vema in the developing spinal cord and optic chiasm resembles the expression patterns of a variety of

182 The chiasm response reveals the temporal order in which the

183 tion zone leads to axons backing up into the chiasm, resulting in circular trajectories and eventual

184 At the optic chiasm, retinal ganglion cell (RGC) axons make the decis

185 At the optic chiasm, retinal ganglion cell axons from each eye conver

186 At the optic chiasm, retinal ganglion cells (RGCs) project ipsi- or c

187 hila homologs of DM-GRASP/BEN/SC1 (irregular chiasm-roughest and dumbfounded) are deleted together.

188 ounded, but not between Hibris and Irregular Chiasm-Roughest.

189 We found that glutamate agonists and optic chiasm stimulation inhibit serotonergic phase advances a

190 his increase, abolishes glutamate- and optic chiasm stimulation-induced phase delays of the SCN circa

191 a3D and sema3E are expressed adjacent to the chiasm, suggesting that they facilitate retinal midline

192 othalamus, and in a site dorsal to the optic chiasm that included the suprachiasmatic nucleus.

193 rapeutic interventions that damage the optic chiasm, the pituitary stalk and the hypothalamic area.

194 The second site is the optic chiasm, the site of retinal axon divergence.

195 al retinal decussation patterns at the optic chiasm: their uncrossed projections are smaller and aris

196 In the chiasm, they are dispersed through the hemichiasm, with

197 t mice initially fail to grow from the optic chiasm to form optic tracts and are delayed temporarily

198 on cell (RGC) axons diverge within the optic chiasm to project to opposite sides of the brain.

199 r to cross or avoid the midline at the optic chiasm to project to targets on both sides of the brain.

200 ephrin-B2 on radial glia cells at the optic chiasm to repulse VT axons away from the midline and int

201 sts, and electrical stimulation of the optic chiasm to SCN brain slices to determine the effect of th

202 tinal ganglion cell (RGC) axons at the optic chiasm to the appropriate hemisphere, a pattern critical

203 rom the area immediately caudal to the optic chiasm to the level of the posterior hypothalamus.

204 hat retinal ganglion cells make at the optic chiasm, to either cross or avoid the midline.

205 axons pathfind normally, but growth from the chiasm toward their targets is impaired, resulting in a

206 RGC axons to progress laterally through the chiasm-tract transition zone to form the optic tract.

207 Here we found that in the chiasm-tract transition zone, axons of CD44/SSEA neurons

208 which the initial pathfinding defect at the chiasm/tract transition zone leads to axons backing up i

209 Stimulation of the optic nerve or chiasm usually evoked a monosynaptic EPSC which was medi

210 y which axons choose their route through the chiasm was also thought to differ between the two major

211 Morphologic analysis of the optic chiasm was based on manual measurement of regions of int

212 inal axon growth and divergence at the optic chiasm, we cocultured mouse retinal and chiasm explants

213 teral and misrouted projections at the optic chiasm were overproduced in Brn3b(-/-) mice but missing

214 Close to the chiasm, where the glial organisation changes and fascicl

215 me axons from each retina cross at the optic chiasm, whereas others do not.

216 we compare guidance mechanisms at the optic chiasm with those in other midline models and highlight

217 of retinal ganglion cell axons at the optic chiasm, with strictly controlled numbers projecting cont

218 regeneration, with axons reaching the optic chiasm within 3 wk.

219 s deficient in GAP-43 have an enlarged optic chiasm within which RGC axons were reportedly stalled.