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MeSH Review

Rhombencephalon

 
 
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Disease relevance of Rhombencephalon

  • We compared the effects of glucose injection with those of saline or mannitol on ischemic brain damage and brain water content in a four-vessel occlusion (4-VO) rat model, which simultaneously causes severe forebrain ischemia and moderate hindbrain ischemia [1].
  • In vitro perturbation of the endogenous trans-interaction between nectin-1 and -3 caused abnormal fasciculation of the commissural axons and impairment of the contacts, and resulted in failure in longitudinal turns of the commissural axons at the contralateral sites of the rat hindbrain [2].
  • Concentrations of NT-4 were detected in regions including the hindbrain and the dorsal root ganglion [3].
  • While nearly one-fourth of hemizygous Bent tail (Bn/Y, Zic3-deficient) mice developed neural tube defects in their midbrain and hindbrain region, the other Bn/Y mice showed apparently normal behaviour in a C57BL/6 genetic background [4].
  • Regulation of NEDD9 may be an important means whereby atRA promotes cell spreading and neurite outgrowth in SH-SY5Y human neuroblastoma cells, and NEDD9 represents a new downstream target of atRA and its receptors in the developing hindbrain [5].
 

Psychiatry related information on Rhombencephalon

 

High impact information on Rhombencephalon

  • Egr2(-/-) mice display disrupted hindbrain segmentation and development, and a block of Schwann-cell differentiation at an early stage [10].
  • The same intersection, when preceded by a third signal, FGF4, which is expressed in the primitive streak, defines an inductive center for hindbrain 5-HT neurons [11].
  • Cdx1 is expressed along the embryonic axis from day 7.5 postcoitum until day 12, by which time the anterior limit of expression has regressed from the hindbrain level to the forelimb bud region [12].
  • Based on an inversion discovered in the original kr allele, we selected a candidate cDNA highly expressed in the developing caudal hindbrain [13].
  • To assess HNF-3 beta function, the gene has been ectopically expressed in the midbrain/hindbrain of transgenic embryos using an En-2 promoter/enhancer [14].
 

Chemical compound and disease context of Rhombencephalon

 

Biological context of Rhombencephalon

  • The identity, expression, and mutant phenotype of kr indicate an early role in axial patterning and provide insights into the molecular and embryologic mechanisms that govern hindbrain and otic development [13].
  • Failure of cranial closure between 9 and 9.5 days postcoitum coincided with increased apoptosis in the midbrain, anterior hindbrain and proximal mesenchyme of the first branchial arch, but did not involve loss of expression of twist or Pax-3, two other regulatory genes known to be required for cranial closure [20].
  • Because Eph receptors and ephrins have complementary expression in many tissues during embryogenesis, bidirectional activation of Eph receptors and ephrin-B proteins could occur at interfaces of their expression domains, for example at segment boundaries in the vertebrate hindbrain [21].
  • The Krox-20 gene encodes a zinc finger transcription factor, which has been shown previously, by targeted inactivation in the mouse, to be required for the development of rhombomeres (r) 3 and 5 in the segmented embryonic hindbrain [22].
  • Mid/hindbrain organizer gene expression, however, continues to be dependent on Gbx2 [23].
 

Anatomical context of Rhombencephalon

 

Associations of Rhombencephalon with chemical compounds

  • Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity [29].
  • Bidirectional signals mediated by membrane-anchored ephrins and Eph receptor tyrosine kinases have important functions in cell-cell recognition events, including those that occur during axon pathfinding and hindbrain segmentation [30].
  • Glucoreceptors controlling feeding and blood glucose: location in the hindbrain [31].
  • Hindbrain GABA receptors influence parasympathetic outflow to the stomach [32].
  • Signaling through RARs is required for patterning along the anteroposterior (A-P) axis, particularly in the hindbrain and posterior, although the absence of RA is required for correct anterior patterning [33].
 

Gene context of Rhombencephalon

  • In mouse embryos homozygous for a Wnt-1-null allele, the midbrain and anterior hindbrain fail to develop [34].
  • A role for Gbx2 in repression of Otx2 and positioning the mid/hindbrain organizer [35].
  • On the basis of these experiments we conclude that the r4-restricted domain of Hoxb2 in the hindbrain is the result of a direct cross-regulatory interaction by Hoxb1 involving vertebrate Pbx proteins as cofactors [36].
  • During mouse hindbrain development, Hoxb3 and Hoxb4 share an expression domain caudal to the boundary between rhombomeres 6 and 7 [37].
  • We further show that the source of Wnt impacting on dorsal otic development emanates from the dorsal hindbrain, and identify Wnt1 and Wnt3a as the specific ligands required for this function [38].
 

Analytical, diagnostic and therapeutic context of Rhombencephalon

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