Hypobaric Preconditioning Modifies Group I mGluRs Signaling in Brain Cortex
| Autor: | D. G. Semenov, M. O. Samoilov, Alexandr V. Belyakov, Tatjana S. Glushchenko, Elzbieta Salinska, Jerzy W. Lazarewicz |
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| Rok vydání: | 2015 |
| Předmět: |
Male
Agonist medicine.medical_specialty medicine.drug_class Receptor Metabotropic Glutamate 5 Phospholipase C beta Piriform Cortex Biology Receptors Metabotropic Glutamate Biochemistry Methoxyhydroxyphenylglycol Cellular and Molecular Neuroscience chemistry.chemical_compound Piriform cortex Internal medicine medicine Animals Inositol 1 4 5-Trisphosphate Receptors Calcium Signaling Rats Wistar Hypoxia Receptor Cerebral Cortex Air Pressure Metabotropic glutamate receptor 5 Inositol trisphosphate General Medicine Rats Up-Regulation medicine.anatomical_structure Endocrinology chemistry Metabotropic glutamate receptor Cerebral cortex Metabotropic glutamate receptor 1 Neuroscience Signal Transduction |
| Zdroj: | Neurochemical Research. 40:2200-2210 |
| ISSN: | 1573-6903 0364-3190 |
| DOI: | 10.1007/s11064-015-1708-9 |
| Popis: | The study assessed involvement of Ca(2+) signaling mediated by the metabotropic glutamate receptors mGluR1/5 in brain tolerance induced by hypoxic preconditioning. Acute slices of rat piriform cortex were tested 1 day after exposure of adult rats to mild hypobaric hypoxia for 2 h at a pressure of 480 hPa once a day for three consecutive days. We detected 44.1 ± 11.6 % suppression of in vitro anoxia-induced increases of intracellular Ca(2+) levels and a fivefold increase in Ca(2+) transients evoked by selective mGluR1/5 agonist, DHPG. Western blot analysis of cortical homogenates demonstrated a 11 ± 4 % decrease in mGluR1 immunoreactivity (IR), and in the nuclei-enriched fraction a 12 ± 3 % increase in IR of phospholipase Cβ1 (PLCβ1), which is a major mediator of mGluR1/5 signaling. Immunocytochemical analysis of the cortex revealed increase in the mGluR1/5 and PLCβ1 IR in perikarya, and a decrease in IR of the neuronal inositol trisphosphate receptors (IP3Rs). We suggest that enhanced expression of mGluR5 and PLCβ1 and potentiation of Ca(2+) signaling may represent pro-survival upregulation of Ca(2+)-dependent genomic processes, while decrease in mGluR1 and IP3R IR may be attributed to a feedback mechanism preventing excessive intracellular Ca(2+) release. |
| Databáze: | OpenAIRE |
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