Neural Activity Triggers Neuronal Oxidative Metabolism Followed by Astrocytic Glycolysis
By K. Kasischke, Harshad D. Vishwasrao, P. Fisher, W. Zipfel, W. Webb. Science, 2004
769 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/46d4c072730e5e61250def2de3a378ad651fe5c2
How researchers see this paper
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In Cellular and Molecular Neuroscience
- Maiken Nedergaard
- Pierre J. Magistretti
- C. Iadecola
- Igor Allaman
- G. Dienel
- Philip Haydon
- Giorgio Carmignoto
- Renaud B. Jolivet
In Molecular Biology
- Pierre J. Magistretti
- Luc Pellerin
- G. Dienel
- Igor Allaman
- Akinobu Suzuki
- Sarah A. Stern
- G. W. Huntley
- R. Walker
In Neurology
- Maiken Nedergaard
- Igor Allaman
- Pierre J. Magistretti
- C. Iadecola
- Philip Haydon
- Giorgio Carmignoto
- Hélène Girouard
- M. Bélanger
Citations in the corpus
- Astrocytic Ca2+ signaling evoked by sensory stimulation in vivo (2006, background): “This notion is supported by new imaging approaches demonstrating that electrical stimulation invariably triggers an increase in astrocytic NADH, indicative of enhanced glycolysi”
- Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation. (2011, background): “…of a rapid and transient decrease of NADH levels in neuronal dendrites, reaching a minimum 10 s after stimulation, 730 Cell Metabolism 14, December 7, 2011 ª2011 Elsevier Inc. followed by a sustained overshoot of NADH levels in astrocytic processes, peaking at 60 s (Kasischke et al., 2004).”
- Mitochondria and neuronal activity. (2007, background): “Moreover, it was proposed that the dip represented a neuronal response, whereas the overshoot was primarily astrocytic, indicating a compartmentalization of oxidative and glycolytic metabolism between neurons and astrocytes (105).”
- Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease. (2006, background): “(38) have investigated the spatial and temporal characteristics of energy metabolism in neurons and astrocytes during activation.”
- Activity‐dependent regulation of energy metabolism by astrocytes: An update (2007, methodology): “Most interestingly, simulation curves for the NADH/NAD1 ratio in astrocytes and neurons are highly consistent with the recent data of Kasischke et al. (2004), with an early neuronal oxidation and a somewhat delayed astrocytic reduction.”
- A cellular perspective on brain energy metabolism and functional imaging. (2015, background): “…of the intrahippocampal Schaffer collateral pathway induces a biphasic NADH fluorescence response consisting of a rapid and transient decrease of NADH levels, reaching a minimum (dip) 10 s after stimulation, followed by a sustained overshoot of NADH, peaking at 60 s (Kasischke et al., 2004).”
- Synaptic energy use and supply. (2012, positive): “The rise of cytoplasmic [Ca2+]i also activates the mitochondrial aspartate-glutamate exchanger aralar (Gellerich et al., 2009), which raises [NADH] in mitochondria and thus supports H+ pumping out across the mitochondrial membrane and subsequent ATP synthesis.”
- Supply and Demand in Cerebral Energy Metabolism: The Role of Nutrient Transporters (2007, background): “This latter event is much slower than neuronal activation and correlates with the slow increase observed in astrocytic nicotinamide adenine dinucleotide levels which was interpreted as an increase in astrocytic G-3-P dehydrogenase activity but does not account for a release in lactate which is nicot”
- Physiology of Astroglia. (2018, neutral): “On the other hand, monitoring NADH levels in hippocampal slices indicated a clear separation between an increase in oxidative neuronal and glycolytic astroglial glucose metabolism (841), yet when these experiments were repeated in vivo, no clear separation was observed (840).”