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Behav Neurosci. 2009 Dec;123(6):1218-25. doi: 10.1037/a0017446.

Deficit in prepulse inhibition in mice caused by dietary n-3 fatty acid deficiency.

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Laboratory of Membrane Biochemistry & Biophysics, National Institutes on Alcohol Abuse & Alcoholism, National Institutes of Health, Bethesda, MD, USA.


Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may be biosynthesized from a precursor alpha-linolenic acid (LNA) or obtained preformed in the diet. Dams were fed four diets with different levels of the various n-3 fatty acids during pregnancy and lactation, and their offspring were weaned to the same diets: "n-3 Deficient," containing (as % total fatty acids) 0.07% of LNA; "Low LNA" (0.4%); "High LNA" (4.8%); and a "DHA + EPA" diet, containing 0.4% of LNA, 2% DHA, and 2% EPA. Sensorimotor gating was measured by prepulse inhibition (PPI) of the acoustic startle response in C57Bl6 mice. The n-3 Deficient and Low LNA diets caused a substantial deficit in PPI compared to the DHA + EPA diet, whereas the High LNA diet induced a less pronounced, but significant reduction of PPI. These are the first data that demonstrate a deficit in sensorimotor gating in rodents caused by an inadequate amount of the n-3 fatty acids in the diet. Our results differentiate the effects of a High LNA diet from one with added EPA and DHA even though the difference in brain DHA content is only 12% between these dietary groups.

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