Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Oct 8;12:335. doi: 10.3389/fncel.2018.00335

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2018 Kovács, Gerevich, Friedman, Otáhal, Prager, Gabriel and Berndt.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Schematic representation of central neuronal energy metabolism (adapted from Bedner et al., 2015). Proton dependent processes are presented in magenta and calcium dependent processes are presented in blue. Glycolysis degrades glucose beginning with hexokinase (hk) dependent phosphorylation to glucose-6-phosphate ending with pyruvate kinase (pk) dependent formation of pyruvate. Pyruvate can by either transformed to lactate by the lactate dehydrogenase (LDH) and be exported from the cell by monocarboxylate transporter (MCT) (anaerobic glycolysis) or taken up into the mitochondria via proton symport by pyruvate transporter (PyrT) with subsequent conversion to Acetyl-Coa by pyruvate dehydrogenase (PDH) for oxidation to CO₂ in the citric acid cycle (CAC) (aerobic glycolysis). The CAC cycle, starting with the formation of citrate (Cit) from oxaloacetate (OA) and acetyl-CoA (ACoA) by citrate synthase (CS) and proceeding via the formation of isocitrate (IsoCit) by aconitase (ACN), α-ketoglutarate (aKG) by isocitrate dehydrogenase (IDH), succinyl-CoA (SucCoA) by α-ketoglutarate dehydrogenase, succinate (Suc) by succinyl-coA synthetase, fumarate (Fum) by succinyldehydrogenase, malate (Mal) by fumerase (FUMR) and the replenishing of OA by malate dehydrogenase (MDH), forms NADH and FADH2 used by the respiratory chain (RC). Complex I-IV of the RC are proton pumps generating the proton motive force that determine the rate of proton-assisted ion transport of Na+, K+, Ca2+ and phosphate (P) across the inner mitochondrial membrane, the rate of the adenine nucleotide transporter (ANT) exchanging mitochondrial ATP against cytosolic ADP and the rate of ATP synthesis by the F0F1-ATPase (F0F1). Shuttling of electrons (NAD-bound hydrogen) between the cytosol and the mitochondrial matrix is catalyzed by the Malate-Asparte shuttle, comprising the malate/α-ketoglutarate carrier (MAC), the mitochondrial and cytosolic aspartate amino transferase (AAT) and the proton driven antiport of glutamate (Glu) and aspartate (Asp) by the aspartate/glutamate carrier (AGC). Besides protons, calcium plays a key role in neuronal energy metabolism as it controls the key mitochondrial dehydrogenase PDH, IDH and KGDH and the rate of electron shuttling by AGC (ARALAR). Calcium uptake into the mitochondrion proceeds in a calcium dependent manner by MCU thereby coupling neuronal excitation with neuronal energy metabolism.