Antibody to NGF inhibits collateral sprouting of septohippocampal fibers following entorhinal cortex lesion in adult rats Journal Articles uri icon

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abstract

  • AbstractWe have used an antiserum raised against mouse 2.5S NGF to examine the involvement of endogenous neurotrophins in the collateral sprouting of septohippocampal fibers in the adult rat brain. The antiserum was administered intraventricularly. Immunocytochemical techniques indicated that the injected antibodies penetrated into brain tissue that included the basal forebrain, cortex, striatum, corpus callosum, and hippocampus. Unilateral lesioning of the entorhinal cortex was done to evoke the sprouting of the cholinergic septohippocampal fibers. At 8 days postlesion, the sprouting was much advanced, as evidenced by an increase in density of the acetylcholinesterase (AChE) staining in the outer molecular layer (OML) of the dentate gyrus and by the associated increase in the absolute number of AChE‐positive fibers in the OML. As well, there was a widening of the inner molecular layer (IML), interpreted as being due to sprouting of noncholinergic axons in that region. In rats injected daily with anti‐NGF or anti‐NGF Fab fragments, no increase in AChE density, or in the population of AChE‐positive fibers, was observed in the OML. In contrast, the widening of the IML seemed to be unaffected by the anti‐NGF treatment. No changes were observed in the AChE related parameters in the dentate gyrus of nonlesioned animals treated similarly for 8 days with anti‐NGF; there was, however, a decrease of choline acetyltransferase (ChAT) immunostaining in the ChAT‐positive cells of the basal forebrain. Our findings and the confirmation that our polyclonal anti‐NGF also recognizes other members of the NGF neurotrophin family, specifically brain‐derived neurotrophic factor and neurotrophin‐3, indicate that at least one of these neurotrophins plays a key role in the collateral sprouting of the cholinergic septohippocampal fibers (but not that presumed to occur within the IML) following an entorhinal cortex lesion. © 1992 Wiley‐Liss, Inc.

publication date

  • December 1992

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