International Meeting for Autism Research: Effects of Prenatal Stress, Prenatal Diet, and Maternal Genotype on Ultrasonic Vocalizations In Mice

Effects of Prenatal Stress, Prenatal Diet, and Maternal Genotype on Ultrasonic Vocalizations In Mice

Thursday, May 12, 2011
Elizabeth Ballroom E-F and Lirenta Foyer Level 2 (Manchester Grand Hyatt)
3:00 PM
K. L. Jones1, M. J. Will1, C. Giesing1, P. M. Hecht1, C. L. Parker1 and D. Q. Beversdorf2, (1)University of Missouri, Columbia, MO, (2)Radiology, Neurology, Psychology, and Thompson Center for Autism and Neurodevelopmental Disorders, University of Missouri, Columbia, MO
Background:  Multiple studies have reported prenatal stress as a potential risk factor for the development of autism spectrum disorder (ASD). In rodents, a significant reduction in sociability is seen in prenatally stressed offspring of serotonin transporter knockout heterozygous (5-HTT +/-) dams.  Additionally, offspring with prenatal maternal diets rich in omega-6 polyunsaturated fatty acids (PUFAs) show decreased social interactions.  Finally, diets rich in omega-3 PUFAs are thought to be neuroprotective and may reduce these effects.  Therefore, it would be important to determine how prenatal stress, genetic susceptibility to stress, and dietary omega-6 and omega-3 PUFAs interact to affect offspring behavior including communication.

Objectives:  In our study, we wished to examine the interaction between the effects of prenatal diet, prenatal stress, and maternal genotype on communicative behavior in newborn offspring in mice.  

Methods:  Pregnant C57BL/6J and 5-HTT +/- dams were placed into a chronic variable stress group or a control group.  Mice placed in the chronic variable stress group were given one stressor per day beginning on gestational day 6 until the birth of the offspring.   Additionally, they received one of four diets beginning 2 weeks before breeding and lasting until offspring were weaned: AIN-93G (control), AIN-93G with added safflower oil (high omega-6 PUFA diet), AIN-93G with added flaxseed oil (added omega-3 PUFAs), and AIN-93G with added pure DHA (pure DHA added omega-3 PUFAs).  We subsequently recorded the ultrasonic vocalizations (USVs) of the offspring on postnatal day 8 as a measure of social communication.

Results:  Our results support our previous findings, in that we observed decreased frequencies and amount of calls of prenatally stressed 5-HTT +/- offspring.  Additionally, we observed effects from the omega-6 diet on the USVs in the offspring, as was observed previously with social behavior.  Finally, addition of omega-3 interacted with these effects.

Conclusions:  This study provides evidence for the roles of maternal genotype, prenatal stress and prenatal diet in offspring sociability in a potential animal model of ASD.  Exploration of the relationship between maternal genotype, prenatal stress, prenatal diet and ASD in humans will be necessary to determine the role of this finding in clinical ASD, and further investigation into the mechanism of action of this effect is warranted.

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