RT Journal Article
SR Electronic
T1 The motor neuron-like cell line NSC-34 and its parent cell line N18TG2 have glycogen that is degraded under cellular stress
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.03.23.004184
DO 10.1101/2020.03.23.004184
A1 Brigitte Pfeiffer-Guglielmi
A1 Ralf-Peter Jansen
YR 2020
UL http://biorxiv.org/content/early/2020/03/25/2020.03.23.004184.abstract
AB Brain glycogen has a long and versatile history: Primarily regarded as an evolutionary remnant, it was then thought of as an unspecific emergency fuel store. A dynamic role for glycogen in normal brain function has been proposed later but exclusively attributed to astrocytes, its main storage site. Neuronal glycogen had long been neglected, but came into focus when sensitive technical methods allowed quantification of glycogen at low concentration range and the detection of glycogen metabolizing enzymes in cells and cell lysates. Recently, an active role of neuronal glycogen and even its contribution to neuronal survival could be demonstrated. Our studies continue these investigations on the function and regulation of neuronal glycogen metabolism. We demonstrate the presence of an active glycogen metabolism in the neuronal cell lines NSC-34 and N18TG2 and the mobilization of the glycogen stores under hypoxia, oxidative and acidic metabolic stress. The key enzyme in glycogen degradation is glycogen phosphorylase. Neurons express only the brain isoform (GPBB) that is supposed to be activated primarily by the allosteric activator AMP and less by covalent phosphorylation via the cAMP cascade. Our results indicate that neuronal glycogen is not degraded upon hormone action but by factors lowering the energy charge of the cells directly.GPBBglycogen phosphorylase brain isoform;GPMMglycogen phosphorylase muscle isoform;GPLLglycogen phosphorylase liver isoform;CNScentral nervous system;PNSperipheral nervous system;DRGdorsal root ganglia;DMEMDulbecco’s modified Eagle’s medium;FCSfetal calf serum