Project description:We are searching for common gene expression alteration in the hippocampus of animal models of learning disabilities and in post-mortem human tissues derived from patients with cognitive deficits. Our study has three phases. In phase I, we want to investigate the changes in gene expression in a transgenic mouse line that shows impairments in hippocampal-dependent learning. These animals are overexpressing the RNA-binding protein HuD in the forebrain under the control of the alpha CAMKinII promoter. For phase II, we plan to characterize the hippocampus of another animal model of learning disabilities: fetal alcohol exposed (FAE) rats. Last, for phase III, we would like to examine gene expression changes in the hippocampus and other tissues from patients with schizophrenia. To test our hypothesis, in phase 2 of our project, we propose to compare the pattern of gene expression in our mouse model with that in the hippocampus of rats prenatally exposed to alcohol (FAE model). Our hypothesis is that learning disabilities have common neural substrates regardless of the origin of the disability being genetic, environmental of a combination of these two. To test this hypothesis, we plan to examine the pattern of gene expression in the hippocampus of animals and humans with cognitive deficits and use bioinformatics tools to identify common changes in gene expression in three of such conditions: a genetic model (HuD transgenic mice), an environmental model (FAE rats) and a model for combined environmental and genetic effects (patients with schizophrenia). All the animals are adult male Sprague-Dawley rats (age 90-100 days). Animals were divided in three diet groups and three experimental treatment conditions (9 conditions altogether). Three groups of pregnant rat dams were placed on different diet regimens: a liquid diet containing 5% alcohol (A) groups, a control group fed an isocaloric liquid diet without alcohol (B) and a group of rats fed lab chow ad libitum (C). Offspring from each of these groups were allowed to grow until adulthood and placed into each of three training groups: a contextual fear conditioned group (1), a non-learning stress control group (2) and a naive/unhandled group (3). Hippocampi were dissected and used to isolate total RNA from each rat diet and training condition. Initially, we will submit 18 samples as follows: 10 samples from training group 1 and 8 samples from training group 3 (training group 2 will be analyzed at a later date). The diet assignment for the 18 samples is: 8 samples from group A, 6 samples of group B and 4 samples of group C. Please note that I was able to enter only the first 8 samples, as the sample list does not hold 18 samples altogether.

Project description:We are searching for common gene expression alteration in the hippocampus of animal models of learning disabilities and in post-mortem human tissues derived from patients with cognitive deficits. Our study has three phases. In phase I, we want to investigate the changes in gene expression in a transgenic mouse line that shows impairments in hippocampal-dependent learning. These animals are overexpressing the RNA-binding protein HuD in the forebrain under the control of the alpha CAMKinII promoter. For phase II, we plan to characterize the hippocampus of another animal model of learning disabilities: fetal alcohol exposed (FAE) rats. Last, for phase III, we would like to examine gene expression changes in the hippocampus and other tissues from patients with schizophrenia. To test our hypothesis, in phase 2 of our project, we propose to compare the pattern of gene expression in our mouse model with that in the hippocampus of rats prenatally exposed to alcohol (FAE model). Our hypothesis is that learning disabilities have common neural substrates regardless of the origin of the disability being genetic, environmental of a combination of these two. To test this hypothesis, we plan to examine the pattern of gene expression in the hippocampus of animals and humans with cognitive deficits and use bioinformatics tools to identify common changes in gene expression in three of such conditions: a genetic model (HuD transgenic mice), an environmental model (FAE rats) and a model for combined environmental and genetic effects (patients with schizophrenia). All the animals are adult male Sprague-Dawley rats (age 90-100 days). Animals were divided in three diet groups and three experimental treatment conditions (9 conditions altogether). Three groups of pregnant rat dams were placed on different diet regimens: a liquid diet containing 5% alcohol (A) groups, a control group fed an isocaloric liquid diet without alcohol (B) and a group of rats fed lab chow ad libitum (C). Offspring from each of these groups were allowed to grow until adulthood and placed into each of three training groups: a contextual fear conditioned group (1), a non-learning stress control group (2) and a naive/unhandled group (3). Hippocampi were dissected and used to isolate total RNA from each rat diet and training condition. Initially, we will submit 18 samples as follows: 10 samples from training group 1 and 8 samples from training group 3 (training group 2 will be analyzed at a later date). The diet assignment for the 18 samples is: 8 samples from group A, 6 samples of group B and 4 samples of group C. Please note that I was able to enter only the first 8 samples, as the sample list does not hold 18 samples altogether. Keywords: dose response

Project description:In our previous study, we reported that a diet rich in antioxidants such as coral calcium hydride (CCH) increased the endogenous antioxidant ability in the hippocampus of rats. We conducted this study to test the hypothesis that diet supplementation with CCH would change the gene expression in rats and to understand how CCH enhances antioxidant ability. We used a DNA array to compare the expression levels in the hippocampus of rats fed with CCH for 2 weeks with those of rats fed a normal diet. Immune response-related genes were down-regulated, while nuclear respiratory factor 2 and aldehyde dehydrogenase 3A were up-regulated. Our findings about the changes in the mRNA levels of these genes well explain the physiological finding of enhanced antioxidant ability in rat brain. CCH was obtained from ICB, Ltd., Sendai, Japan, and coral calcium (CC) was purchased from Coralbio, Okinawa, Japan. Male Wistar rats were acquired from Kyudo, Co., Ltd. and maintained at the Experimental Animal Center of the University of Miyazaki at a controlled ambient temperature of 23 ¬¨¬± 1 ¬¨‚àûC and 50 ¬¨¬± 10% relative humidity. The Committee for Ethics on Animal Experiments, Faculty of Medicine, University of Miyazaki, Japan, reviewed and approved the experimental design. Six-week-old male Wistar rats (n = 8) were assigned to 2 groups: standard diet-fed group (CE-2, Clea Japan, Inc., Tokyo, Japan) and CCH-fed group. The CCH diet was standard CE-2 feed supplemented with 0.1% CCH powder. Inhibition of accelerated aging and an increase in the in vivo antioxidant ability was observed in SAM/P-8 mice fed a diet supplemented with 0.1% CCH. In accordance with these reports, the CCH concentration used in our study was set at 0.1%.The animals were killed by cervical dislocation at the age of 8 weeks. They were decapitated and the hippocampi were removed and rapidly frozen in liquid nitrogen. The hippocampi were then homogenized with a conventional rotor-stator homogenizer. Total RNA was then extracted from the tissues by using the RNeasy Lipid Tissue Mini Kit (Qiagen, Valencia, CA).

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Transcription profiling of rat hippocampus from fetal alcohol exposed rats

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