Depolarization induces insulin-like growth factor binding protein-2 expression in vivo via NMDA receptor stimulation
| Autor: | I.A Langmoen, A. C. Sandberg Nordqvist, Staffan Holmin, Tiit Mathiesen |
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| Rok vydání: | 2001 |
| Předmět: |
Male
medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Gene Expression Stimulation In situ hybridization Biology Receptors N-Methyl-D-Aspartate Membrane Potentials Rats Sprague-Dawley Endocrinology Downregulation and upregulation Internal medicine medicine Animals RNA Messenger Insulin-Like Growth Factor I In Situ Hybridization TUNEL assay Growth factor Brain Depolarization Molecular biology Rats Insulin-Like Growth Factor Binding Protein 2 Insulin-Like Growth Factor Binding Protein 4 Astrocytes Cortical spreading depression NMDA receptor Dizocilpine Maleate Excitatory Amino Acid Antagonists |
| Zdroj: | Growth Hormone & IGF Research. 11:399-406 |
| ISSN: | 1096-6374 |
| Popis: | The effect of depolarization and N -methyl- D -aspartate (NMDA) receptor blockade on insulin-like growth factor-I (IGF-I), IGF binding protein-2 (IGFBP-2) and IGFBP-4 expression was analysed in vivo. Depolarization was induced in adult rat brains by applying 3 M KCl to the exposed cortex for 10 min. A subgroup of animals also received daily injections of MK-801. Four days after KCl exposure, the brains were analysed by in situ hybridization, immunohistochemistry and TUNEL. A significant upregulation of IGFBP-2 mRNA and protein was detected in astrocytes after KCl exposure This upregulation was reduced by MK-801 treatment. No alterations in IGF-I or IGFBP-4 mRNA levels were noted. We did not detect TUNEL positive cells, morphological signs of necrosis or apoptosis, or neuronal loss in the depolarized zone. Taken together, these findings indicate that upregulation of IGFBP-2 by depolarization is mediated by NMDA receptors, and, as no neuronal damage was detected, astrocytic NMDA receptors may be responsible for this upregulation. |
| Databáze: | OpenAIRE |
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