scholarly journals N-3 fatty acids, neuronal activity and energy metabolism in the brain

2012 ◽  
Vol 19 (4) ◽  
pp. 238-244 ◽  
Author(s):  
Emilie Harbeby ◽  
Fabien Pifferi ◽  
Mélanie Jouin ◽  
Hélène Pélerin ◽  
Sébastien Tremblay ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-22 ◽  
Author(s):  
Alexander Panov ◽  
Zulfiya Orynbayeva ◽  
Valentin Vavilin ◽  
Vyacheslav Lyakhovich

In this review, we analyze the current hypotheses regarding energy metabolism in the neurons and astroglia. Recently, it was shown that up to 20% of the total brain’s energy is provided by mitochondrial oxidation of fatty acids. However, the existing hypotheses consider glucose, or its derivative lactate, as the only main energy substrate for the brain. Astroglia metabolically supports the neurons by providing lactate as a substrate for neuronal mitochondria. In addition, a significant amount of neuromediators, glutamate and GABA, is transported into neurons and also serves as substrates for mitochondria. Thus, neuronal mitochondria may simultaneously oxidize several substrates. Astrocytes have to replenish the pool of neuromediators by synthesis de novo, which requires large amounts of energy. In this review, we made an attempt to reconcileβ-oxidation of fatty acids by astrocytic mitochondria with the existing hypothesis on regulation of aerobic glycolysis. We suggest that, under condition of neuronal excitation, both metabolic pathways may exist simultaneously. We provide experimental evidence that isolated neuronal mitochondria may oxidize palmitoyl carnitine in the presence of other mitochondrial substrates. We also suggest that variations in the brain mitochondrial metabolic phenotype may be associated with different mtDNA haplogroups.


OCL ◽  
2018 ◽  
Vol 25 (4) ◽  
pp. D409 ◽  
Author(s):  
Stephen C. Cunnane

Optimal brain performance is intimately linked to the brain’s Yin and the Yang − the balance between its structure and its energy metabolism. This relationship is clearly exemplified in infant brain development and in Alzheimer’s disease, and probably also applies to human brain evolution. In these examples, redundant pathways help achieve this important balance. For instance, the key structural lipid for the brain, docosahexaenoic acid (DHA), is supplied to the infant brain from at last three overlapping sources: (i) milk; (ii) infant’s own fat stores and (iii) by some endogenous synthesis from α-linolenic acid (ALA) or eicosapentaenoic acid (EPA). On the energy side, glucose is normally the brain’s main fuel but under conditions of prolonged starvation, it can be almost totally replaced by the ketone bodies, acetoacetate and β-hydroxybutyrate. When ketones are present in the blood they spare glucose uptake by the brain because they are actually the brain’s preferred fuel and are essential for normal infant brain development. The redundant sources of ketones are long chain fatty acids (including the relatively ketogenic ALA) in infant stores, and medium chain triglycerides (MCT) in milk. Besides infancy, nowhere is the strain on the brain’s balance between yin and yang more apparent than in Alzheimer’s disease (AD). One of the reasons why attempts to treat AD have largely failed could well be because chronically inadequate glucose supply to some areas of the brain on the order of 10% is present in people at risk of AD long before cognitive decline begins. However, brain ketone uptake is still normal even in moderately advanced AD. Hence, treatments that ignore the brain energy (glucose) deficit in AD would be predicted to fail, but treatments that attempt to rescue brain fuel availability via ketones would be predicted to have a better chance of succeeding. By analogy to ketones sparing glucose for brain energy metabolism, perhaps ALA or EPA entering the brain can help spare (conserve) DHA for its structural role. If so, it would not necessarily be futile to transport ALA and EPA into the brain just to β-oxidize the majority afterwards; DHA sparing as well as ketone production could be important beneficiaries.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Susumu Takahashi ◽  
Takumi Hombe ◽  
Riku Takahashi ◽  
Kaoru Ide ◽  
Shinichiro Okamoto ◽  
...  

Abstract Background Salmonids return to the river where they were born in a phenomenon known as mother-river migration. The underpinning of migration has been extensively examined, particularly regarding the behavioral correlations of external environmental cues such as the scent of the mother-river and geomagnetic compass. However, neuronal underpinning remains elusive, as there have been no biologging techniques suited to monitor neuronal activity in the brain of large free-swimming fish. In this study, we developed a wireless biologging system to record extracellular neuronal activity in the brains of free-swimming salmonids. Results Using this system, we recorded multiple neuronal activities from the telencephalon of trout swimming in a rectangular water tank. As proof of principle, we examined the activity statistics for extracellular spike waveforms and timing. We found cells firing maximally in response to a specific head direction, similar to the head direction cells found in the rodent brain. The results of our study suggest that the recorded signals originate from neurons. Conclusions We anticipate that our biologging system will facilitate a more detailed investigation into the neural underpinning of fish movement using internally generated information, including responses to external cues.


1990 ◽  
Vol 109 (5) ◽  
pp. 682-685
Author(s):  
V. A. Sorokoumov ◽  
Yu. Ya. Kislyakov ◽  
E. L. Pugacheva ◽  
E. R. Barantsevich ◽  
V. A. Grantyn'

1967 ◽  
Vol 45 (6) ◽  
pp. 853-861 ◽  
Author(s):  
W. Thompson

The hydrolysis of monophosphoinositide by soluble extracts from rat brain is described. Diglyceride and inositol monophosphate are liberated along with a small amount of free fatty acids. Hydrolysis of the lipid is optimal at pH 5.4 in acetate buffer. The reaction is stimulated by calcium ions or by high concentration of monovalent cations and, to a less extent, by long-chain cationic amphipathic compounds. Enzyme activity is lost on dialysis of the brain extract and can be restored by diffusible factor(s). Some differences in the conditions for hydrolysis of mono- and tri-phosphoinositides are noted.


Renal Failure ◽  
1999 ◽  
Vol 21 (5) ◽  
pp. 551-554
Author(s):  
Hiroshi Tanaka ◽  
Hideki Hirakata ◽  
Hidetoshi Kanai ◽  
Itsuko Ishida ◽  
Masatoshi Fujishima

1966 ◽  
Vol 101 (3) ◽  
pp. 591-597 ◽  
Author(s):  
R M O'Neal ◽  
R E Koeppe ◽  
E I Williams

1. Free glutamic acid, aspartic acid, glutamic acid from glutamine and, in some instances, the glutamic acid from glutathione and the aspartic acid from N-acetyl-aspartic acid were isolated from the brains of sheep and assayed for radioactivity after intravenous injection of [2-(14)C]glucose, [1-(14)C]acetate, [1-(14)C]butyrate or [2-(14)C]propionate. These brain components were also isolated and analysed from rats that had been given [2-(14)C]propionate. The results indicate that, as in rat brain, glucose is by far the best precursor of the free amino acids of sheep brain. 2. Degradation of the glutamate of brain yielded labelling patterns consistent with the proposal that the major route of pyruvate metabolism in brain is via acetyl-CoA, and that the short-chain fatty acids enter the brain without prior metabolism by other tissue and are metabolized in brain via the tricarboxylic acid cycle. 3. When labelled glucose was used as a precursor, glutamate always had a higher specific activity than glutamine; when labelled fatty acids were used, the reverse was true. These findings add support and complexity to the concept of the metabolic; compartmentation' of the free amino acids of brain. 4. The results from experiments with labelled propionate strongly suggest that brain metabolizes propionate via succinate and that this metabolic route may be a limited but important source of dicarboxylic acids in the brain.


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