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Transient Increase of Cyclic AMP Induced by Glutamate in Cultured Neurons from Rat Spinal Cord
Author(s) -
Tsuji Koji,
Nakamura Yoichi,
Ogata Tadanori,
Shibata Taihoh,
Kataoka Kiyoshi
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65041816.x
Subject(s) - spinal cord , glutamate receptor , transient (computer programming) , neuroscience , chemistry , biology , biochemistry , computer science , receptor , operating system
We demonstrated that glutamate increased the cyclic AMP level in cultured neurons from rat spinal cord. A bath application of glutamate (300 µ M ) elicited a rapid increase of the cyclic AMP concentration reaching a level three times as high as the basal level in ∼3 min, and its content then decreased to the control level in 15 min. The increase was not observed in a Ca 2+ ‐free medium and was inhibited by an antagonist of NMDA receptors or a voltage‐sensitive Ca 2+ channel blocker. Preincubation with W7 also inhibited the glutamate‐evoked cyclic AMP increase. NMDA, aspartate, and high‐K + conditions also induced a cyclic AMP increase; however, a decreasing phase did not follow. The decreasing phase was observed when (2 S ,1′ S ,2′ S )‐2‐(carboxycyclopropyl)‐glycine, a potent agonist for metabotropic glutamate receptors, was combined with NMDA. These results suggest that the cyclic AMP increase is mediated by a Ca 2+ influx via both NMDA receptors and voltage‐sensitive Ca 2+ channels followed by an activation of the Ca 2+ /calmodulin system, and the decreasing phase observed in the case of glutamate exposure is due to the activation of the metabotropic glutamate receptors.