Does a High-Fat Maternal Diet Affect Spatial Learning and Memory Abilities in Rat Offspring?

2015 ◽  
Vol 39 ◽  
pp. S21 ◽  
Author(s):  
Jamie-Lee Robb ◽  
Erika Lui ◽  
Isabelle Messa ◽  
Derrick Yeung ◽  
Jonathan Thacker ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-16
Author(s):  
Wycliffe Makori Arika ◽  
Cromwell Mwiti Kibiti ◽  
Joan Murugi Njagi ◽  
Mathew Piero Ngugi

Chronic exposures to high-fat diets are linked to neuropathological changes that culminate in obesity-related cognitive dysfunction and brain alteration. Learning, memory performance, and executive function are the main domains affected by an obesogenic diet. There are limited effective therapies for addressing cognitive deficits. Thus, it is important to identify additional and alternative therapies. In African traditional medicine, Gnidia glauca has putative efficacy in the management of obesity and associated complications. The use of Gnidia glauca is largely based on its long-term traditional use. Its therapeutic application has not been accompanied by sufficient scientific evaluation to validate its use. Therefore, the current study sought to explore the modulatory effects of dichloromethane leaf extracts of Gnidia glauca on cognitive function in the high-fat diet- (HFD-) induced obese rats. Obesity was induced by feeding the rats with prepared HFD and water ad libitum for 6 weeks. The in vivo antiobesity effects were determined by oral administration of G. glauca at dosage levels of 200, 250, and 300 mg/kg body weight in HFD-induced obese rats from the 6th to the 12th weeks. The Lee obesity index was used as a diagnostic criterion of obesity. The Morris water maze was employed to test spatial learning and memory retention in rats. The results indicated that Gnidia glauca showed potent antiobesity effects as indicated in the reduction of body weight and obesity index in extract-treated rats. Moreover, Gnidia glauca exhibited cognitive-enhancing effects in obese rats. The positive influences on cognitive functions might be attributed to the extracts’ phytochemicals that have been suggested to confer protection against obesity-induced oxidative damage, reduction of central inflammation, and increased neurogenesis. The therapeutic effects observed suggest that Gnidia glauca might be an alternative to current medications for the symptomatic complications of obesity, such as learning and memory loss. Further studies are therefore needed to establish its toxicity profiles.


2020 ◽  
Vol 107 (2) ◽  
pp. 209-219
Author(s):  
F.S. Sajjadi ◽  
F. Aghighi ◽  
Z. Vahidinia ◽  
A. Azami-Tameh ◽  
M. Salami ◽  
...  

AbstractIntroductionExposure to noise stress during early life may permanently affect the structure and function of the central nervous system. The aim of this study was to evaluate the effects of prenatal exposure to urban traffic noise on the spatial learning and memory of the rats' offspring and the expression of glucocorticoid receptors (GRs) in their hippocampi.MethodsThree g\roups of pregnant rats were exposed to recorded urban traffic noise for 1, 2 or 4 h/day during the last week of pregnancy. At the age of 45 days, their male offspring were introduced to the Morris water maze (MWM) for assessment of spatial learning and memory. The corticosterone levels were measured in the offspring's sera by radioimmunoassay, and the relative expression of glucocorticoid and mineralocorticoid receptors (MRs) in their hippocampi was evaluated via RT-PCR.ResultsFacing urban traffic noise for 2 and 4 h/day during the third trimester of pregnancy caused the offspring to spend more time and to travel a larger distance than the controls to find the target platform. Analogously, these two groups were inferior to their control counterparts in the probe test. Also, prenatal noise stress elevated the corticosterone concentration in the sera of the rats' offspring and dose-dependently decreased the relative expression of the mRNA of both GRs and MRs in their hippocampi.ConclusionsUrban traffic noise exposure during the last trimester of pregnancy impairs spatial learning and memory of rat offspring and reduces GRs and MRs gene expression in the hippocampus.


Neuroreport ◽  
2020 ◽  
Vol 31 (3) ◽  
pp. 265-273
Author(s):  
Mei-Hsin Hsu ◽  
Jiunn-Ming Sheen ◽  
Yu-Chieh Chen ◽  
Hong-Ren Yu ◽  
You-Lin Tain ◽  
...  

2014 ◽  
Vol 306 (8) ◽  
pp. R527-R537 ◽  
Author(s):  
Kathleen C. Page ◽  
Elizabeth K. Jones ◽  
Endla K. Anday

We tested the hypothesis that excess saturated fat consumption during pregnancy, lactation, and/or postweaning alters the expression of genes mediating hippocampal synaptic efficacy and impairs spatial learning and memory in adulthood. Dams were fed control chow or a diet high in saturated fat before mating, during pregnancy, and into lactation. Offspring were weaned to either standard chow or a diet high in saturated fat. The Morris Water Maze was used to evaluate spatial learning and memory. Open field testing was used to evaluate motor activity. Hippocampal gene expression in adult males was measured using RT-PCR and ELISA. Offspring from high fat-fed dams took longer, swam farther, and faster to try and find the hidden platform during the 5-day learning period. Control offspring consuming standard chow spent the most time in memory quadrant during the probe test. Offspring from high fat-fed dams consuming excess saturated fat spent the least. The levels of mRNA and protein for brain-derived neurotrophic factor and activity-regulated cytoskeletal-associated protein were significantly decreased by maternal diet effects. Nerve growth factor mRNA and protein levels were significantly reduced in response to both maternal and postweaning high-fat diets. Expression levels for the N-methyl-d-aspartate receptor (NMDA) receptor subunit NR2B as well as synaptophysin were significantly decreased in response to both maternal and postweaning diets. Synaptotagmin was significantly increased in offspring from high fat-fed dams. These data support the hypothesis that exposure to excess saturated fat during hippocampal development is associated with complex patterns of gene expression and deficits in learning and memory.


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