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Título: | Insulin-like growth factor I modulates c-Fos induction and astrocytosis in response to neurotoxic insult |
Autor: | Fernández García, Ana María CSIC ORCID ; García-Estrada, J.; García-Segura, Luis M. CSIC ORCID; Torres Alemán, Ignacio CSIC ORCID | Fecha de publicación: | 1996 | Editor: | Elsevier | Citación: | Neuroscience 76: 117-122 (1996) | Resumen: | Insulin-like growth factor I participates in the cellular response to brain insult by increasing its messenger RNA expression and/or protein levels in the affected area. Although it has been suggested that insulin-like growth factor I is involved in a variety of cellular responses leading to homeostasis, mechanisms involved in its possible trophic effects are largely unknown. Since activation of c-Fos in postmitotic neurons takes place both in response to insulin-like growth factor I and after brain injury, we have investigated whether this early response gene may be involved in the actions of insulin-like growth factor I after brain insult. Partial deafferentation of the cerebellar cortex by 3-acetylpyridine injection elicited c-Fos protein expression on both Purkinje and granule cells of the cerebellar cortex. This neurotoxic insult also triggered gliosis, as determined by an increased number of glial fibrillary acidic protein-positive cells (reactive astrocytes) in the cerebellar cortex. When 3-acetylpyridine-injected animals received a continuous intracerebellar infusion of either a peptidic insulin-like growth factor I receptor antagonist or an insulin-like growth factor I antisense oligonucleotide for two weeks through an osmotic minipump, c-Fos expression was obliterated while reactive gliosis was greatly increased. On the contrary, continuous infusion of insulin-like growth factor I significantly decreased reactive gliosis without affecting the increase in c-Fos expression. These results indicate that insulin-like growth factor I is involved in both the neuronal (c-Fos) and the astrocytic (glial fibrillary acidic protein) activation in response to injury. | URI: | http://hdl.handle.net/10261/67576 | DOI: | 10.1016/S0306-4522(96)00395-8 | Identificadores: | doi: 10.1016/S0306-4522(96)00395-8 issn: 0306-4522 |
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