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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: J Neurochem. 2011 May 19;118(1):140–152. doi: 10.1111/j.1471-4159.2011.07289.x

Fig. 6. Hypothetical scheme summarizing the effects of pathological cell swelling on glutamate-glutamine cycle in the brain tissue.

Fig. 6

(a) Under physiological conditions extracellular glutamate (GLU) is recycled via the concerted work of glutamate uptake via GLAST-1 and GLT-1 transporters, conversion to glutamine (GLN) by glutamine synthetase (GS), and glutamine release and uptake by astrocytic SNAT-3 and neuronal SNAT-1. In neurons, glutamine is hydrolyzed to glutamate by phosphate-activated glutaminase (PAG). (b) Astrocytic cell swelling opens the glutamate-permeable channel VRAC and strongly inhibits activity of GS, resulting in lower levels of glutamine production and export. Other abbreviations: AMPA, NMDA, KA, ionotropic glutamate receptors; α-KG, α-ketoglutarate; GDH, glutamate dehydrogenase; vGluT, vesicular glutamate transporters. Note that for simplicity this diagram omits a number of alternative glutamine transporters and important metabolic enzymes.