Intracellular calcium mobilization triggered by a glutamate receptor in rat cultured hippocampal cells

• Published in: The Journal of physiology Vol. 414; no. 1; pp. 539 - 548
• Main Authors: Furuya, S, Ohmori, H, Shigemoto, T, Sugiyama, H
• Format: Journal Article
• Language: English
• Published: Oxford The Physiological Society 01.07.1989; Blackwell
• Subjects: Animals; Animals, Newborn; Biological and medical sciences; Calcium - metabolism; Cells, Cultured; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; Fundamental and applied biological sciences. Psychology; Glutamates - pharmacology; Glutamic Acid; Hippocampus - cytology; Hippocampus - metabolism; Intracellular Membranes - metabolism; Oxadiazoles - pharmacology; Pertussis Toxin; Potassium - pharmacology; Quisqualic Acid; Rats; Receptors, Glutamate; Receptors, Neurotransmitter - metabolism; Vertebrates: nervous system and sense organs; Virulence Factors, Bordetella - pharmacology; Human; Cell culture; Agonist; Calcium; Rat; Rodentia; Central nervous system; Activation; Glutamate receptor; Proteins; Vertebrata; Mammalia; Newborn; Aminoacid; Nervous receptor; Cell; Hippocampus; Release
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.1989.sp017702

1. Intracellular free calcium ([Ca2+]i) was monitored by means of Fura-2 fluorescence measurements in hippocampal cells in primary cultures from newborn rats. 2. In external media containing 200 microM-DL-2-amino-5-phosphonovalerate and 1 mM-kynurenate, but no added Ca2+, an increase in [Ca2+]i was observed in 30-40% of cells examined in response to quisqualate or L-glutamate. 3. Under such conditions, [Ca2+]i often increased gradually with a latency of a few seconds after application of the agonists. 4. Pre-treatment of the cultured cells with pertussis toxin reduced the extent of quisqualate-stimulated [Ca2+]i increase in Ca2+-free media, but the percentage of the responsive cells was not affected appreciably. 5. It is concluded that quisqualate and L-glutamate can trigger the release of Ca2+ from intracellular Ca2+ stores, most likely by activating a glutamate receptor coupled to a pertussis toxin-sensitive G-protein.