Event Title
Crazy Rats and Cholinergic Resolutions: Applications of Dietary Choline in a Genetic Rat Model of Schizophrenia
Location
Diamond 122
Start Date
1-5-2014 9:00 AM
End Date
1-5-2014 10:30 AM
Project Type
Presentation- Restricted to Campus Access
Description
Schizophrenia is a rare debilitating brain disorder caused by genetic and environmental factors. About 3 million people in the United States suffer with schizophrenia during their lifetime. A growing body of research implicates a gene called disordered in schizophrenia-1, or DISC1, in the expression of schizophrenic symptoms. Recently, experimental investigation of the gene has been made possible by a rat model of DISC1, in which rats lack both copies of the DISC1 allele. While mouse models of similar genetics research have existed for decades, the rat model is relatively new and opens a door to more reliable behavioral experimentation. Characterization of behavioral traits in the DISC1 knockout rat is valuable on its own; however, the present study also explores the role of dietary choline, an essential nutrient, in protecting against various deficits the knockout rats genetic predisposition to schizophrenia. Especially when used as a supplement prenatally or early in development, choline defends against memory loss, anxiety, and depression among other insults. In the present study, after an adolescent choline-supplemented diet manipulation, 32 Sprague-Dawley rats were evaluated in a battery of behavioral measures to compare motor behavior, social interaction, anxiety, and object memory. Results showed a strong effect of genotype in all measures. Choline supplementation did not rescue genetic knockouts behavioral outcomes. In some cases, choline supplemented resulted in more impairments in the DISC1 knockout rats. While diet results are unclear and open to interpretation, DISC1 genotype results successfully mirrored human positive symptoms of schizophrenia, validating the DISC1 model for use in future research.
Faculty Sponsor
Martha Arterberry
Sponsoring Department
Colby College. Psychology Dept.
CLAS Field of Study
Social Sciences
Event Website
http://www.colby.edu/clas
ID
299
Crazy Rats and Cholinergic Resolutions: Applications of Dietary Choline in a Genetic Rat Model of Schizophrenia
Diamond 122
Schizophrenia is a rare debilitating brain disorder caused by genetic and environmental factors. About 3 million people in the United States suffer with schizophrenia during their lifetime. A growing body of research implicates a gene called disordered in schizophrenia-1, or DISC1, in the expression of schizophrenic symptoms. Recently, experimental investigation of the gene has been made possible by a rat model of DISC1, in which rats lack both copies of the DISC1 allele. While mouse models of similar genetics research have existed for decades, the rat model is relatively new and opens a door to more reliable behavioral experimentation. Characterization of behavioral traits in the DISC1 knockout rat is valuable on its own; however, the present study also explores the role of dietary choline, an essential nutrient, in protecting against various deficits the knockout rats genetic predisposition to schizophrenia. Especially when used as a supplement prenatally or early in development, choline defends against memory loss, anxiety, and depression among other insults. In the present study, after an adolescent choline-supplemented diet manipulation, 32 Sprague-Dawley rats were evaluated in a battery of behavioral measures to compare motor behavior, social interaction, anxiety, and object memory. Results showed a strong effect of genotype in all measures. Choline supplementation did not rescue genetic knockouts behavioral outcomes. In some cases, choline supplemented resulted in more impairments in the DISC1 knockout rats. While diet results are unclear and open to interpretation, DISC1 genotype results successfully mirrored human positive symptoms of schizophrenia, validating the DISC1 model for use in future research.
https://digitalcommons.colby.edu/clas/2014/program/323