<i>N</i>-Docosahexaenoylethanolamide promotes development of hippocampal neurons

Kim, Hee Yong; Moon, Hee Sun; Cao, Dehua; Lee, Jeongrim; Kevala, Karl; Jun, Sang Beom; Lovinger, David M.; Akbar, Mohammed; Huang, Boji

doi:10.1042/bj20102118

Cited by 107 publications

(124 citation statements)

References 36 publications

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“…It became apparent by the end of the 1990s that the requirement for DHA probably is the primary reason why -3 fatty acids are essential ( 86 ). This tentative conclusion was supported by subsequent fi ndings indicating that DHA enhances cognition ( 87 ) and synaptic function ( 88 ), and that it is converted to lipid mediators that facilitate the resolution of acute infl ammation ( 89 ), provide neuroprotection ( 90 ), and promote hippocampal development ( 91 ).…”

Section: Essential Fatty Acids In Humanssupporting

confidence: 57%

Discovery of essential fatty acids

Spector

Kim

2015

Journal of Lipid Research

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172

131

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Journal of Lipid Research Volume 56, 2015 11polyunsaturated fatty acid containing two double bonds (18:2 -6), cured this defi ciency disease and, therefore, was an essential fatty acid ( 2 ). These two seminal papers are now regarded as classics in biochemistry ( 3 ), but they initially met with considerable skepticism ( 4 ). To understand why, one must appreciate the paradigm-changing nature of the discovery and the stature of the experts whose views concerning dietary fat were being challenged by Burr's fi ndings. VIEWS ON THE ROLE OF DIETARY FAT IN THE EARLY 20th CENTURYProteins and carbohydrates were known to be indispensable dietary components by the fi rst decade of the 20th century. However, dietary fat was not considered to be essential because fatty acids were known to be synthesized from carbohydrates. The evidence concerning fat was not defi nitive due to the inability to completely extract fat from the other dietary components using the methods available in the early 1900s, and the experimental fat-free diets of that era contained traces of residual fat.Two of the most prominent physiological chemists of the early 20th century, Thomas B. Osborne of the Connecticut Agricultural Experiment Station and Lafayette B. Mendel of the Sheffi eld Scientifi c School at Yale University, began their studies on the role of dietary fat in 1912. Osborne and Mendel were working collaboratively in New Haven and were already recognized world-wide for their pioneering studies on dietary proteins. Their initial fi ndings indicated that rats gained weight normally when fed a fatfree food mixture, and they concluded that "true fats" are not required for growth ( 5 ). However, Osborne and Mendel were aware of the work of Wilhelm Stepp in Strasbourg, who found that a lipoid present in egg yolk was an essential nutrient for mice ( 6, 7 ). MacArthur and Luckett at the University of Illinois also reported that a lipoid extracted from egg yolk was necessary for optimum growth of mice ( 8 ).Abstract Dietary fat was recognized as a good source of energy and fat-soluble vitamins by the fi rst part of the 20th century, but fatty acids were not considered to be essential nutrients because they could be synthesized from dietary carbohydrate. This well-established view was challenged in 1929 by George and Mildred Burr who reported that dietary fatty acid was required to prevent a defi ciency disease that occurred in rats fed a fat-free diet. They concluded that fatty acids were essential nutrients and showed that linoleic acid prevented the disease and is an essential fatty acid. The Burrs surmised that other unsaturated fatty acids were essential and subsequently demonstrated that linolenic acid, the omega-3 fatty acid analog of linoleic acid, is also an essential fatty acid. The discovery of essential fatty acids was a paradigm-changing fi nding, and it is now considered to be one of the landmark discoveries in lipid research.

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Section: Essential Fatty Acids In Humanssupporting

confidence: 57%

Discovery of essential fatty acids

Spector

Kim

2015

Journal of Lipid Research

Self Cite

172

131

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“…Here, we point out that the period of exposure to n-3 PUFAs might be critical as a previous work showed that DHA-depletion in fetal hippocampi from E2 to E16 resulted in decrease in the number of synapses (Cao et al, 2009). Additionally, experiments performed in vitro on hippocampal neurons in culture showed that application of 1µM of DHA increased significantly the total number of synapses compared to control cultures (Kim et al, 2011). This confirmed previous results from Cao et al showing that 10 days of in vitro supplementation with DHA at 1µM significantly promotes synaptogenesis (Cao et al, 2009).…”

Section: )mentioning

confidence: 81%

Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment

Delpech

Thomazeau

Madore

et al. 2015

Neuropsychopharmacol

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Dietary n-3 polyunsaturated fatty acids (PUFAs) are critical components of inflammatory response and memory impairment. However, the mechanisms underlying the sensitizing effects of low n-3 PUFAs in the brain for the development of memory impairment following inflammation are still poorly understood. In this study, we examined how a 2-month n-3 PUFAs deficiency from pre-puberty to adulthood could increase vulnerability to the effect of inflammatory event on spatial memory in mice. Mice were given diets balanced or deficient in n-3 PUFAs for a 2-month period starting at post-natal day 21, followed by a peripheral administration of lipopolysaccharide (LPS), a bacterial endotoxin, at adulthood. We first showed that spatial memory performance was altered after LPS challenge only in n-3 PUFA-deficient mice that displayed lower n-3/n-6 PUFA ratio in the hippocampus. Importantly, long-term depression (LTD), but not long-term potentiation (LTP) was impaired in the hippocampus of LPS-treated n-3 PUFA-deficient mice. Proinflammatory cytokine levels were increased in the plasma of both n-3 PUFA-deficient and n-3 PUFA-balanced mice. However, only n-3 PUFA-balanced mice showed an increase in cytokine expression in the hippocampus in response to LPS. In addition, n-3 PUFA-deficient mice displayed higher glucocorticoid levels in response to LPS as compared with n-3 PUFA-balanced mice. These results indicate a role for n-3 PUFA imbalance in the sensitization of the hippocampal synaptic plasticity to inflammatory stimuli, which is likely to contribute to spatial memory impairment.

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“…Current knowledge on the role of DHEA in the central nervous system, especially in the amygdala, is limited. DHEA has been found to promote synaptic development and glutamatergic synaptic activity in hippocampal neurons (Kim et al, 2011a;Kim et al, 2011b). DHEA oxidative metabolism products have also been associated with antiinflammatory and neuroprotective properties (Yang et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Endogenous cannabinoids in amygdala and hippocampus in post-mortem brains of Cloninger type 1 and 2 alcoholics

Kärkkäinen

Lehtonen

Laukkanen

et al. 2013

Alcohol

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Accumulating evidence continues to link certain aspects of the endogenous cannabinoid (EC) system with alcohol dependence, negative reinforcement learning and the modulation of stress response.Specific alterations in brain regions that are related to stress and negative reinforcement learning have been reported to exist in Cloninger type 1 and 2 alcoholics. To study possible differences in profiles of ECs between Cloninger type 1 (n=9), type 2 (n=8) alcoholics and non-alcoholic control subjects (n=10), we analyzed post-mortem amygdala and hippocampus brain samples for several ECs by quantitative liquid chromatography with triple quadrupole mass spectrometric detection. A significant difference was found between these three groups in terms of EC profiles in the amygdala (p = 0.037).In particular, this difference was prominent for variations in docosahexaenoylethanolamine levels, which were significantly higher in type 1 alcoholics (p = 0.022) when compared to controls. There was also a large negative correlation between anandamide concentration and mGlu1/5 receptor density in the hippocampus of Cloninger type 1 alcoholics (R=-0.88, p=0.002), which was not seen in type 2 alcoholics or in controls. Although preliminary, and from relatively small diagnostic groups, these results suggest that the EC profile may be altered in the hippocampus and amygdala of type 1 alcoholics.

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N-Docosahexaenoylethanolamide promotes development of hippocampal neurons

Cited by 107 publications

References 36 publications

Discovery of essential fatty acids

Discovery of essential fatty acids

Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment

Endogenous cannabinoids in amygdala and hippocampus in post-mortem brains of Cloninger type 1 and 2 alcoholics

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