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Elevated expression of B‐50 (GAP‐43)‐mRNA in a subpopulation of olfactory bulb mitral cells following axotomy
Author(s) -
Verhaagen J.,
Zhang Y.,
Hamers F. P. T.,
Gispen W. H.
Publication year - 1993
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490350206
Subject(s) - axotomy , olfactory bulb , gap 43 protein , biology , central nervous system , lesion , downregulation and upregulation , olfactory system , messenger rna , anatomy , neuroscience , microbiology and biotechnology , pathology , immunology , immunohistochemistry , medicine , gene , biochemistry
Neurons in the central nervous system regenerate poorly or not at all. In contrast neurons of the peripheral nervous system have the ability to regrow their nerve fibers over considerable distances. Previously it has been suggested that the absence of the reinduction of the expression of growth associated proteins such as B‐50 (GAP43) may be an important factor in the differential response of CNS and PNS neurons to injury. We studied B‐50(GAP43) mRNA expression following lesioning of a class of CNS neurons, the olfactory bulb mitral cells. Expression of B‐50 mRNA in approximately 40% of the mitral cells was upregulated in response to transection of their axons in the lateral olfactory tract (LOT). Enhanced expression persisted for 10 days postlesion but had virtually declined to control levels by 4 weeks after the lesion. A large proportion of the mitral cells gradually degenerated subsequent to LOT transection. Thus a subpopulation of mitral cells maintains their ability to upregulate B‐50, a protein characteristic of growing axons, but enhanced B‐50 expression is not accompanied by regeneration of the severed LOT. © 1993 Wiley‐Liss, Inc.