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Increased expression of specific recognition molecules by retinal ganglion cells and by optic pathway glia accompanies the successful regeneration of retinal axons in adult zebrafish
Author(s) -
Bernhardt R.R.,
Tongiorgi E.,
Anzini P.,
Schachner M.
Publication year - 1996
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19961209)376:2<253::aid-cne7>3.0.co;2-2
Subject(s) - axotomy , biology , optic nerve , microbiology and biotechnology , regeneration (biology) , zebrafish , retina , giant retinal ganglion cells , neuroscience , retinal ganglion cell , retinal regeneration , optic tract , muller glia , anatomy , stem cell , progenitor cell , genetics , gene
Retinal ganglion cells (RGCs) in adult zebrafish can regenerate their axons. We show that successful axonal regeneration is accompanied by the re‐expression by RGCs of mRNAs encoding specific recognition molecules that are expressed at high levels in the larval retina but are down‐regulated in the adult. Message levels for l1.1 and l1.2 (two homologs of mammalian L1), n‐cam (homologous to mammalian N‐CAM), beta3 (related to the beta3 and beta2 subunits of mammalian Na, K‐ATPase), and tn‐c (homologous to mammalian tenascin‐C) were high in larval RGCs undergoing axonogenesis and low in adult RGCs. After an optic nerve crush, axotomized adult RGCs showed increased levels of l1.1, l1.2, and n‐cam mRNA expression, whereas the levels of beta3 and tn‐cmRNA remained unchanged. The optic nerve crush also induced the expression of some of these mRNAs in the optic nerve and tract where they are not normally detectable. This lesion induced up‐regulation by presumptive glia was observed for l1.1, l1.2, n‐cam and beta3 but not for tn‐c. The combination of a neuronal (intrinsic) response to axotomy with an environmental (extrinsic) response may be an important determinant allowing for the successful axonal regeneration. © 1996 Wiley‐Liss, Inc.