Cholecystokinin-induced protection of cultured cortical neurons against glutamate neurotoxicity
Autor: | Kumi Ozaki, Akinori Akaike, Setsuko Miura, Tomoko Yoshinaga, Yutaka Tamura, Yuko Sato, Rika Matsuoka |
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Rok vydání: | 1991 |
Předmět: |
medicine.drug_class
Glutamic Acid Pharmacology Biology digestive system Neuroprotection Devazepide Receptors N-Methyl-D-Aspartate Glutamates Pregnancy medicine Neurotoxin Animals Molecular Biology Ceruletide Cells Cultured Cholecystokinin Cerebral Cortex Neurons Benzodiazepinones Cell Death General Neuroscience Phenylurea Compounds digestive oral and skin physiology Glutamate receptor Neurotoxicity Trypan Blue Receptor antagonist medicine.disease Rats NMDA receptor Female Receptors Cholecystokinin Neurology (clinical) Neuroscience Excitatory Amino Acid Antagonists hormones hormone substitutes and hormone antagonists Developmental Biology |
Zdroj: | Brain research. 557(1-2) |
ISSN: | 0006-8993 |
Popis: | The effects of cholecystokinin (CCK) on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Brief exposure of glutamate followed by an incubation with normal solution for more than 60 min reduced cell viability by 60–70%, compared with control values. Glutamate-induced neurotoxicity was significantly inhibited by MK-801 and ketamine, which are non-competitive blockers of N-methyl- d -aspartate (NMDA) receptors. Octapeptide CCK-8S and CCK-related decapeptide ceruletide at concentrations of 10−9−10−7 M dose-dependently reduced glutamate-induced neurotoxicity. A desulfated analog CCK-8NS, which acts selectively as an antagonist of CCKB receptors, also reduced glutamate neurotoxicity. The neuroprotective effects of CCK were antagonized by L-365260, a CCKB receptor antagonist, but not by L-364718, a CCKA receptor antagonist. These results suggest that CCK protects cortical neurons against NMDA receptor-mediated glutamate neurotoxicity via CCKB receptors. |
Databáze: | OpenAIRE |
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