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The aim of the present study was to investigate the possible relationship between the levels of various brain fatty acids and learning indices in aged (22-23 months old) and young (2-3 months old) female C57BL/6 mice classified as “good” or “poor” learners basing on their performance in a spatial learning task: the Morris water-maze. The levels of several fatty acids including palmitic, stearic, oleic, linoleic, arachidonic (AA), and docosahexaenoic acid (DHA) were measured by gas chromatography in brain tissue samples from four different brain areas: hippocampus, cortex, striatum and hypothalamus. The results of behavioural tests confirmed a decline in learning skills with age. However, a great individual variation was revealed in learning scores between aged subjects indicating that biological aging is not always parallel to chronological aging. The relative levels of palmitic, stearic, oleic, linoleic, arachidonic, and DHA acids in the four examined brain structures were very similar. Interestingly, except hypothalamus, no significant relation has been found between the brain levels of DHA omega-3 acid and the animal’s age or cognitive status. This finding contributes to the current debate on the value of DHA supplementation as an effective protective treatment against aging and dementia. The only significant correlation between learning performance and the brain fatty acid levels was found for arachidonic acid in the young mice hippocampus, structure known to be critical for spatial learning and memory. AA level was significantly lower in young “good learners” as compared to both young “poor learners” and old “good learners” with young “good learners” showing significantly better performance than the two other groups. These results are discussed in the context of recent reports about elevated AA levels in Alzheimer’s dementia.
It is well known that the fetal ethanol exposure and prenatal stress may have adverse effects on brain development. Interestingly, some morphological and functional recovery from their teratogenic effects that take place during brain maturation. However, mechanisms that underlie this recovery are not fully elucidated. The aim of this study was to examine whether the postnatal attenuation of fetal alcohol – and maternal stress-induced morphological and functional deficits correlates with compensatory changes in the expression/activation of the brain proteins involved in inflammation, cell survival and apoptosis. In this project, we investigated the hippocampus which belongs to the brain regions most susceptible to the adverse effects of prenatal ethanol exposure. Pregnant rat dams were administered ethanol (A) or isocaloric glucose solution (IC) by a gastric intubation during gestational days 7-20. The pure control group received ad libitum laboratory chow and water with no other treatment. The hippocampi of fetal-ethanol and control pups were examined at the postnatal day (PD)1, PD10, PD30 and PD60. Moderate fetal-ethanol exposure and prenatal intubation stress caused a significant increase in molecular factors relating to inflammation (iNOS) and cell survival/apoptosis pathways (PTEN, GSK-3 and ERK) at birth, with a rapid compensation from these developmental deficits upon removal of alcohol at PD10. Indeed, an increase in ERK1/2 and JNK1/2 activation at PD30 was observed with ethanol consumption. It indicates that the recovery process in A and IC brains started soon after the birth upon the ethanol and stressor withdrawal and continued until the adulthood.
Diclofenac sodium (DS) acts as a potent cyclooxygenase inhibititor, reducing arachidonic acid release and prostaglandins formation. It is commonly used as a non-steroid anti-infl ammatory drug and the potential adverse effects of its administration during pregnancy are of medical and public concern. In the present study, the DS in a dose of 1 mg/kg/day was subcutaneously injected to the pregnant Wistar rats throughout 5–20 gestational days. One group of 4-week old pups was sacrifi ced and the counts of principal neurons in cerebellum and hippocampus were done using stereological methods. Another group of pups was subjected to a battery of behavioral tasks. A signifi cant decrease in the total number of Purkinje cells but not CA pyramidal neurons was observed in the drug-treated juvenile pups. No substantial between-group differences were found in most of the applied behavioral tasks including plus maze anxiety test, and learning/memory tasks such as 12-arm radial maze and the Morris water maze, the latter run both under allo- and idiothetic stimulus conditions. Only in the Open Field test, fetal DS male but not female pups showed slower rate of habituation compared to controls. The obtained results indicated that the moderate doses of DS administered between 5–20 gestation days in rats equivalent of the second half of the 1st and the whole 2nd trimester in human) resulted in some neuronal losses which, however, had no adverse behavioral impact.
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