title: Graded expression patterns of ephrin-As in the superior colliculus after lesion of the adult mouse optic nerve.
abstract: The idea has been put forward that molecules and mechanisms acting during development are re-used during regeneration in the adult, for example in response to traumatic injury in order to re-establish the functional integrity of neuronal circuits. Members of the Eph family of receptor tyrosine kinases and their 'ligands', the ephrins, play a prominent role during development of the retinocollicular projection in rodents, where EphA receptors and ephrin-As are expressed in gradients in both the retina and the superior colliculi (SC). We were interested in investigating whether EphA family members are also expressed or re-expressed in the adult after optic nerve lesion, since the presence of axon guidance information is an important prerequisite for a topographically appropriate re-connection by retinal ganglion cell (RGC) axons. This analysis was encouraged by results showing that RGC axons do not exert guidance preferences in response to membranes from adult unlesioned SC, but in response to membranes from the adult deafferented SC. We found a graded expression pattern of ephrin-As in the SC both before and after deafferentation, which was remarkably similar to those found during development. EphA receptor levels were reduced in the SC after deafferentation and the expression patterns of the EphB family were not changed. In particular, the presence of a graded ephrin-A expression in the deafferented SC suggests that - if robust regeneration of RGC axons can be achieved - topographic guidance information as a likely requirement for a functionally successful re-establishment of the retinocollicular projection is available.
authors.affiliation: Department of Physical Biology, Max-Planck-Institute for Developmental Biology, Spemannstrasse 35, 72076, Tübingen, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Knöll
authors.forename: S
authors.initials: S
authors.lastname: Isenmann
authors.forename: E
authors.initials: E
authors.lastname: Kilic
authors.forename: J
authors.initials: J
authors.lastname: Walkenhorst
authors.forename: S
authors.initials: S
authors.lastname: Engel
authors.forename: J
authors.initials: J
authors.lastname: Wehinger
authors.forename: M
authors.initials: M
authors.lastname: Bähr
authors.forename: U
authors.initials: U
authors.lastname: Drescher
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology; D005075:Biological Evolution; D003714:Denervation; D036383:Ephrin-A2; D036384:Ephrin-A3; D036385:Ephrin-A4; D036386:Ephrin-A5; D036388:Ephrin-B2; D015870:Gene Expression; D017403:In Situ Hybridization; D008024:Ligands; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009416:Nerve Regeneration; D009900:Optic Nerve / Q000502:physiology* / Q000601:surgery; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism*; D036141:Receptor, EphA7; D036224:Receptor, EphB4; D036081:Receptors, Eph Family; D012160:Retina / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000502:physiology; D013477:Superior Colliculi / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*; D014795:Visual Pathways
chemical_list: D036383:Ephrin-A2; D036384:Ephrin-A3; D036385:Ephrin-A4; D036386:Ephrin-A5; D036388:Ephrin-B2; D008024:Ligands; D008565:Membrane Proteins; D012333:RNA, Messenger; D014157:Transcription Factors; D020794:Receptor Protein-Tyrosine Kinases; D036141:Receptor, EphA7; D036224:Receptor, EphB4; D036081:Receptors, Eph Family