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The Journal of Neuroscience, February 15, 2000, 20(4):1342-1347

Neuronal Pyruvate Carboxylation Supports Formation of Transmitter Glutamate

Bjørnar Hassel and Anders Bråthe

Norwegian Defense Research Institute, Division for Environmental Toxicology, N-2027 Kjeller, Norway

Release of transmitter glutamate implies a drain of -ketoglutarate from neurons, because glutamate, which is formed from -ketoglutarate, is taken up by astrocytes. It is generally believed that this drain is compensated by uptake of glutamine from astrocytes, because neurons are considered incapable of de novo synthesis of tricarboxylic acid cycle intermediates, which requires pyruvate carboxylation. Here we show that cultured cerebellar granule neurons form releasable [¹⁴C]glutamate from H¹⁴CO₃ and [1-¹⁴C]pyruvate via pyruvate carboxylation, probably mediated by malic enzyme. The activity of pyruvate carboxylation was calculated to be approximately one-third of the pyruvate dehydrogenase activity in neurons. Furthermore, intrastriatal injection of NaH¹⁴CO₃ or [1-¹⁴C]pyruvate labeled glutamate better than glutamine, showing that pyruvate carboxylation occurs in neurons in vivo. This means that neurons themselves to a large extent may support their release of glutamate, and thus entails a revision of the current view of glial-neuronal interactions and the importance of the glutamine cycle.

Key words: transmitter glutamate; pyruvate carboxylation; CO₂ fixation; malic enzyme; anaplerosis; 3-nitropropionic acid

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Copyright © 2000 Society for Neuroscience  0270-6474/00/2041342-06$05.00/0

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