Format

Send to

Choose Destination
See comment in PubMed Commons below
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.

Author information

1
Laboratory of Membrane Biochemistry & Biophysics, National Institutes on Alcohol Abuse & Alcoholism, National Institutes of Health, Bethesda, MD, USA. idahms@martek.com

Abstract

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.

PMID:
20001105
PMCID:
PMC2852869
DOI:
10.1037/a0017446
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for American Psychological Association Icon for PubMed Central
    Loading ...
    Support Center