| First Author | Baeza-Lehnert F | Year | 2019 |
| Journal | Cell Metab | Volume | 29 |
| Issue | 3 | Pages | 668-680.e4 |
| PubMed ID | 30527744 | Mgi Jnum | J:273870 |
| Mgi Id | MGI:6282808 | Doi | 10.1016/j.cmet.2018.11.005 |
| Citation | Baeza-Lehnert F, et al. (2019) Non-Canonical Control of Neuronal Energy Status by the Na(+) Pump. Cell Metab 29(3):668-680.e4 |
| abstractText | Neurons have limited intracellular energy stores but experience acute and unpredictable increases in energy demand. To better understand how these cells repeatedly transit from a resting to active state without undergoing metabolic stress, we monitored their early metabolic response to neurotransmission using ion-sensitive probes and FRET sensors in vitro and in vivo. A short theta burst triggered immediate Na(+) entry, followed by a delayed stimulation of the Na(+)/K(+) ATPase pump. Unexpectedly, cytosolic ATP and ADP levels were unperturbed across a wide range of physiological workloads, revealing strict flux coupling between the Na(+) pump and mitochondria. Metabolic flux measurements revealed a "priming" phase of mitochondrial energization by pyruvate, whereas glucose consumption coincided with delayed Na(+) pump stimulation. Experiments revealed that the Na(+) pump plays a permissive role for mitochondrial ATP production and glycolysis. We conclude that neuronal energy homeostasis is not mediated by adenine nucleotides or by Ca(2+), but by a mechanism commanded by the Na(+) pump. |
