Differences in the release ofl-glutamate andd-aspartate from primary neuronal chick cultures |
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Authors: | Lena Lewin Mats-Olof Mattsson Åke Sellström |
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Affiliation: | 1. Department of Cellular and Development Biology, Ume? University, S-901 87, UME?, Sweden 2. Division of Biomedicine, National Defence Research Establishment, S-901 82, UME?, Sweden
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Abstract: | Primary neuronal cultures were made from eight-day-old embryonic chick telencephalon. Ten-day-old cultures were used to study the release ofd-[3H]aspartate andl-[3H]glutamate. Thed-[3H]aspartate release was stimulated by increasing potassium concentrations, but it was not calcium dependent. In contrast, the potassium dependentl-[3H]glutamate release was calcium dependent, and furthermorel-[3H]glutamate release was optimal at potassium concentrations<30 mM. The inhibitors of glutamate uptake, dihydrokainate and 1-aminocyclobutane-trans-1,3-dicarboxylic acid (CACB), also referred to as cis-1-aminocyclobutane-1,3-dicarboxylate, were used in the release experiments. Dihydrokainate had no effect on aspartate release, whereas CACB increased both the basal efflux ofd-[3H]aspartate and the potassium evoked release. CACB had no effect on the potassium stimulatedl-glutamate release. We believe thatl-glutamate is released mainly by a vesicular mechanism from the presumably glutamatergic neurons present in our culture.d-aspartate release observed by us, could be mediated by a transporter protein. The cellular origin of this release remains to be assessed. |
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Keywords: | font-variant:small-caps" >l-Glutamate font-variant:small-caps" >d-aspartate neuronal culture release dihydrokainate 1-aminocyclobutane-trans-1,3-dicarboxylic acid (CACB) |
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