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Glutamate‐induced calcium increase in myotubes depends on up‐regulation of a sodium‐dependent transporter
Author(s) -
Frank Claudio,
Giammarioli Anna Maria,
Falzano Loredana,
Fiorentini Carla,
Rufini Stefano
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03200-3
Subject(s) - transporter , chemistry , calcium , depolarization , glutamate receptor , biochemistry , adenosine , biophysics , microbiology and biotechnology , biology , gene , receptor , organic chemistry
We report a study on the regulation by 2‐chloro adenosine (2CA) of a glutamate (Glu) transporter in myogenic C2C12 cells. Long‐term 2CA exposition significantly increased the V max of the Glu transporter. Moreover, 2CA‐treated cells responded to Glu challenge by a rapid and transient increase in their intracellular calcium level. The above reported effects were totally abolished by treating C2C12 cells with the Na + ‐dependent Glu transporter inhibitors DL ‐threo‐b‐hydroxyaspartic acid and L ‐ trans ‐pyrrolidine‐2,4‐dicarboxylic acid. We propose that the possible link between the Glu uptake increase and the Glu induction of calcium rise could be the depolarizing currents carried by Na + coupled with transporter activity.

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