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. 2016 Apr 18;9:40. doi: 10.1186/s13041-016-0223-5

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© Zheng et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 7 — Summary of the metabolic changes in the hippocampus tissue of db/db mice with cognitive decline including glucose metabolism and glutamate–glutamine cycle compared with WT mice. In hyperglycemia circumstance, glycolysis is elevated, while aerobic oxidation is inhibited. As precursor for glutamate, reduction of TCA intermediates, combining with lower levels of glutaminase (GLS) and glutamate decarboxylase (GAD) in neuron, all contributes to the decreased level of glutamate and GABA. The reduced glutamate level, which is consistent with attenuation of postsynaptic glutamate receptors, i.e. N-methyl-D-aspartate (NMDA) subtype, and inhibition of synaptic long-term potentiation (LTP), may contribute to the pathogenesis of diabetes-associated cognitive decline. Keys: glutamate transporter 1 (GLT-1), glutamate aspartate transporter 1 (GLAST-1), sodium-coupled neutral amino acid transporters (SNATs), glucose transporter (Glut 1)