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Insulin‐like growth factor‐I counteracts bFGF‐induced survival of nitric oxide synthase (NOS)‐positive spinal cord neurons after target‐lesion in vivo
Author(s) -
Blottner Dieter,
Baumgarten H. G.
Publication year - 1992
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.490320403
Subject(s) - basic fibroblast growth factor , nitric oxide synthase , spinal cord , neurotrophic factors , in vivo , fibroblast growth factor , growth factor , biology , endocrinology , nitric oxide , medicine , neuroscience , biochemistry , receptor , microbiology and biotechnology
We have used nitric oxide synthase (NOS) histochemistry as a perikaryal viability marker to trace the retrograde reaction of spinal cord intermediolateral (IML) sympathoadrenal projection (SAP)‐neurons to target‐removal, i.e., selective adrenomedullectomy and local administration of either insulin‐like growth factor‐I (IGF‐I), basic fibroblast growth factor (bFGF) or a combination of both. Counting of NOS‐positive preganglionic spinal cord neurons 4 weeks post surgery indicated that more than 80% of stained neurons were lost from the IML‐cell column. This percentage loss corresponds to the numerical loss of NOS‐stained SAP‐neurons labeled retrogradely with Fast‐blue prior to adrenomedullectomy. Basic FGF‐supplementation at the site of lesion resulted in maintenance of the majority of NOS‐positive IML‐neurons, a finding confirmed by the survival rate of Fast‐blue prelabeled SAP‐neurons. Thus, besides maintenance of the structural integrity of SAP‐neurons, bFGF prevents loss of intracellular NOS‐activity which may reflect unaltered cell metabolism (and function) of these neurons following target‐removal in vivo. By contrast, IGF‐I failed to alter the rate of disappearance of NOS‐staining and labeling index of neurons within the IML‐cell column postlesion, suggesting that IGF‐I is not neurotrophic for SAP‐neurons by itself. Combined treatment with both factors resulted in a more widespread loss of NOS‐stained and Fast‐blue‐prelabeled SAP‐neurons than registered after bFGF‐only treatment. No co‐trophic effect of bFGF and IGF‐I was evident; rather, the pronounced bFGF‐induced rescuing effect was significantly suppressed by exogenous IGF‐I in vivo, supporting the idea that this or another molecule induced by the treatment enhances rather than prevents retrograde degeneration and neuronal death within the adult lesioned IML‐adrenal pathway. © 1992 Wiley‐Liss, Inc.