Friday, May 21, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
1:00 PM
Background: Mouse models of autism provide translational strategies to test hypotheses about causes and to develop treatments. While assays are available for social interaction and repetitive behaviors in mice, there is a need for relevant methods to assess communication impairments. We are currently developing behavioral tools to assay olfactory communication in mice. SHANK genes, which code for synaptic scaffolding proteins, have been implicated in autism spectrum disorders.
Objectives: The present study examines Shank1 null mutant mice for interest in social olfactory cues and potential olfactory communication impairments.
Methods: Scent marks deposited by a male mouse in response to a spot of female urine in an open field were quantitated in Shank1 null mutants, heterozygotes, and wildtype littermates, using methods previously described (Arakawa et al., 2007; Roullet et al., 2009). Ultrasonic vocalizations emitted by the subjects and locomotor activity were simultaneously recorded as previously described (Roullet et al., 2009; Wöhr et al., 2009). Scent marking, locomotor activty and time spent were measured for both the entire open field and in a proximal zone within 10 cm of the female urine spot.
Results: Shank1 -/- mice deposited a lower number of scent marks within 10 cm around the female urine and spent less time within this proximal area. Scores for the entire open field showed no genotype differences in the total number of scent marks deposited in the presence of the female urine, nor in the total locomotor activity. In the absence of a female urine spot, Shank1 -/- had lower locomotor activity, consistent with the previous report (Hung et al., 2008) and our companion poster (Silverman et al., 2009). When comparing the total number of ultrasonic vocalizations, genotype differences were not significant. All genotypes started to emit calls about 1 minute after exposure to female urine.
Conclusions: Our results suggest that Shank1 null mutant mice have reduced interest in female urinary pheronomones, which could indicate deficits in olfactory communication.
References:
Arakawa H., Arakawa K., Blanchard D.C. and Blanchard R.J. (2007) Scent marking behavior in male C57BL/6J mice: sexual and developmental determination. Behav Brain Res, 182, 73-79.
Hung A.Y., Futai K., Sala C., Valtschanoff J.G., Ryu J., Woodworth M.A., Kidd F.L., Sung C.C., Miyakawa T., Bear M.F., Weinberg R.J., Sheng M. (2008) Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1. J Neurosci, 13;28(7):1697-708.
Roullet F.I., Wöhr M. and Crawley J.N. (2009) Scent marking and countermarking behaviors as a measure of olfactory communication in the BTBR T+tf/J inbred strain, a mouse model of autism. Society for Neuroscience, Chicago-USA Oct. 17-21, 2009
Silverman J.L., Barkan C. L., Tolu S. S., Turner S.M., Saxena R., Diagne D. D., Hung A.Y., Sheng M. and Crawley J.N. (2009) Behavioral phenotypes of Shank1 mutant mice. The 9th Annual International Meeting for Autism Research (IMFAR), Philadelphia, Pennsylvania, USA, May 20-22, 2010
Wöhr M., Roullet F.I., Hung A.Y., Sheng M. and Crawley J.N. (2009) Reduced ultrasonic vocalizations in mice lacking Shank1. Society for Neuroscience, Chicago-USA Oct. 17-21, 2009
Objectives: The present study examines Shank1 null mutant mice for interest in social olfactory cues and potential olfactory communication impairments.
Methods: Scent marks deposited by a male mouse in response to a spot of female urine in an open field were quantitated in Shank1 null mutants, heterozygotes, and wildtype littermates, using methods previously described (Arakawa et al., 2007; Roullet et al., 2009). Ultrasonic vocalizations emitted by the subjects and locomotor activity were simultaneously recorded as previously described (Roullet et al., 2009; Wöhr et al., 2009). Scent marking, locomotor activty and time spent were measured for both the entire open field and in a proximal zone within 10 cm of the female urine spot.
Results: Shank1 -/- mice deposited a lower number of scent marks within 10 cm around the female urine and spent less time within this proximal area. Scores for the entire open field showed no genotype differences in the total number of scent marks deposited in the presence of the female urine, nor in the total locomotor activity. In the absence of a female urine spot, Shank1 -/- had lower locomotor activity, consistent with the previous report (Hung et al., 2008) and our companion poster (Silverman et al., 2009). When comparing the total number of ultrasonic vocalizations, genotype differences were not significant. All genotypes started to emit calls about 1 minute after exposure to female urine.
Conclusions: Our results suggest that Shank1 null mutant mice have reduced interest in female urinary pheronomones, which could indicate deficits in olfactory communication.
References:
Arakawa H., Arakawa K., Blanchard D.C. and Blanchard R.J. (2007) Scent marking behavior in male C57BL/6J mice: sexual and developmental determination. Behav Brain Res, 182, 73-79.
Hung A.Y., Futai K., Sala C., Valtschanoff J.G., Ryu J., Woodworth M.A., Kidd F.L., Sung C.C., Miyakawa T., Bear M.F., Weinberg R.J., Sheng M. (2008) Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1. J Neurosci, 13;28(7):1697-708.
Roullet F.I., Wöhr M. and Crawley J.N. (2009) Scent marking and countermarking behaviors as a measure of olfactory communication in the BTBR T+tf/J inbred strain, a mouse model of autism. Society for Neuroscience, Chicago-USA Oct. 17-21, 2009
Silverman J.L., Barkan C. L., Tolu S. S., Turner S.M., Saxena R., Diagne D. D., Hung A.Y., Sheng M. and Crawley J.N. (2009) Behavioral phenotypes of Shank1 mutant mice. The 9th Annual International Meeting for Autism Research (IMFAR), Philadelphia, Pennsylvania, USA, May 20-22, 2010
Wöhr M., Roullet F.I., Hung A.Y., Sheng M. and Crawley J.N. (2009) Reduced ultrasonic vocalizations in mice lacking Shank1. Society for Neuroscience, Chicago-USA Oct. 17-21, 2009