The Use of Hippocampal Slices for the Study of Energy Metabolism

2003 ◽  
pp. 99-132 ◽  
Author(s):  
Tim S. Whittingham
1992 ◽  
Vol 17 ◽  
pp. 69
Author(s):  
Makoto Nabetani ◽  
Yukihiro Yamada ◽  
Shinji Kawai ◽  
Masahiko Yonetani ◽  
Satoshi Takada ◽  
...  

2016 ◽  
Author(s):  
Anton Ivanov ◽  
Anton E Malkov ◽  
Svetlna Buldakova ◽  
Misha Zilberter ◽  
Yuri Zilberter

Major risk factors for neurodegenerative diseases share brain hypometabolism as one common outcome. In turn, many neurodegenerative pathologies result in brain hypometabolism; both epilepsy and Alzheimer's disease are characterised by disruptions in glucose metabolism. However, the causative link between energy shortage and neuronal pathologies in these disease has remained elusive. Using real-time brain slice recordings of energy metabolism parameter (NAD(P)H, FAD, pO2 and extracellular glucose) transients in response to network activation, we found that induced epileptic seizures and amyloid-beta peptide both result in similar and long-lasting disruptions of neuronal energy metabolism, suggesting a common path of action. In addition, we found that in both cases, subsequent addition of pyruvate, the principal mitochondrial fuel possessing multiple neuroprotective properties, completely normalised the disputed energy state. Our data suggests that energy metabolism disruptions underlie the initiation and progression of neurodegenerative diseases.


2013 ◽  
Vol 34 (3) ◽  
pp. 397-407 ◽  
Author(s):  
Anton I Ivanov ◽  
Anton E Malkov ◽  
Tatsiana Waseem ◽  
Marat Mukhtarov ◽  
Svetlana Buldakova ◽  
...  

Network activation triggers a significant energy metabolism increase in both neurons and astrocytes. Questions of the primary neuronal energy substrate (e.g., glucose vs. lactate) as well as the relative contributions of glycolysis and oxidative phosphorylation and their cellular origin (neurons vs. astrocytes) are still a matter of debates. Using simultaneous measurements of electrophysiological and metabolic parameters during synaptic stimulation in hippocampal slices from mature mice, we show that neurons and astrocytes use both glycolysis and oxidative phosphorylation to meet their energy demands. Supplementation or replacement of glucose in artificial cerebrospinal fluid (ACSF) with pyruvate or lactate strongly modifies parameters related to network activity-triggered energy metabolism. These effects are not induced by changes in ATP content, pHi, [Ca2+]i or accumulation of reactive oxygen species. Our results suggest that during network activation, a significant fraction of NAD(P)H response (its overshoot phase) corresponds to glycolysis and the changes in cytosolic NAD(P)H and mitochondrial FAD are coupled. Our data do not support the hypothesis of a preferential utilization of astrocyte-released lactate by neurons during network activation in slices—instead, we show that during such activity glucose is an effective energy substrate for both neurons and astrocytes.


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