Abstract
To investigate the effects of omega-3 fatty acid deficiency on phosphatidylinositol signaling in brain, myo-inositol (mI) concentrations were determined in the prefrontal cortex (PFC) of omega-3 fatty acid deficient rats by in vivo proton magnetic resonance spectroscopy ((1)H-MRS). To generate graded deficits in PFC docosahexaenoic acid (22:6n-3) (DHA) composition, perinatal and postweaning alpha-linolenic acid (18:3n-3) (ALA) deficiency models were used. Adult male rats were scanned in a 7T Bruker Biospec system and a (1)H-MRS spectrum acquired from the bilateral medial PFC. Rats were then challenged with SKF83959, a selective agonist at phosphoinositide (PI)-coupled dopamine D(1) receptors. Postmortem PFC fatty acid composition was determined by gas chromatography. Relative to controls, PFC DHA composition was significantly reduced in adult postweaning (-27%) and perinatal (-65%) ALA-deficiency groups. Basal PFC mI concentrations were significantly reduced in the perinatal deficiency group (-21%, P = 0.001), but not in the postweaning deficiency group (-1%, P = 0.86). Among all rats, DHA composition was positively correlated with mI concentrations and the mI/creatine (Cr) ratio. SKF83959 challenge significantly increased mI concentrations only in the perinatal deficiency group (+16%, P = 0.02). These data demonstrate that perinatal deficits in cortical DHA accrual significantly and selectively reduce mI concentrations and augment receptor-generated mI synthesis.
Highlights
To investigate the effects of omega-3 fatty acid deficiency on phosphatidylinositol signaling in brain, myoinositol concentrations were determined in the prefrontal cortex (PFC) of omega-3 fatty acid deficient rats by in vivo proton magnetic resonance spectroscopy (1H-MRS)
This study determined the effects of graded PFC docosahexaenoic acid (22:6n-3) (DHA) deficits on PFC mI concentrations by in vivo 1H-MRS
A principle finding is that perinatal a-linolenic acid (18:3n-3) (ALA) deficiency resulting in large PFC DHA deficits (265%) was associated with significantly lower basal mI concentrations in the adult rat PFC (221%)
Summary
To investigate the effects of omega-3 fatty acid deficiency on phosphatidylinositol signaling in brain, myoinositol (mI) concentrations were determined in the prefrontal cortex (PFC) of omega-3 fatty acid deficient rats by in vivo proton magnetic resonance spectroscopy (1H-MRS). PFC DHA composition was significantly reduced in adult postweaning (227%) and perinatal (265%) ALA-deficiency groups. Perinatal n-3 fatty acid deficiency selectively reduces myo-inositol levels in the adult rat PFC: an in vivo 1H-MRS study. Perinatal or postweaning dietary ALA deficiency significantly reduces cortical DHA composition in the adult rat brain [7, 8]. Electrostatic binding of MARCKS with membrane phosphatidylserine serves to inhibit phospholipase C (PLC)-mediated phosphatidylinositol (PI) hydrolysis by sequestering phosphatidylinositol 4,5bisphosphate in lateral membrane domains [13] These findings suggest that reductions in membrane phosphatidylserine content, and associated reductions in MARCKS membrane binding, would dysregulate PI second messenger signaling activity in the DHA-deficient rat brain. Prior studies have found that increasing omega-3 fatty acid intake down-regulates basal and stimulated PI hydrolysis in peripheral tissues [14–16], there is currently nothing about the effects of DHA deficiency on PI signaling in brain
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