Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.

Autism is a neurodevelopmental disorder with a strong genetic component. Core symptoms are abnormal reciprocal social interactions, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior with restricted interests. Candidate genes for autism include the SHANK ge...

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Autores principales: Markus Wöhr, Florence I Roullet, Albert Y Hung, Morgan Sheng, Jacqueline N Crawley
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Publicado: Public Library of Science (PLoS) 2011
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spelling oai:doaj.org-article:4059565f040041e597f0906290f714dd2021-11-18T06:52:20ZCommunication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.1932-620310.1371/journal.pone.0020631https://doaj.org/article/4059565f040041e597f0906290f714dd2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21695253/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Autism is a neurodevelopmental disorder with a strong genetic component. Core symptoms are abnormal reciprocal social interactions, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior with restricted interests. Candidate genes for autism include the SHANK gene family, as mutations in SHANK2 and SHANK3 have been detected in several autistic individuals. SHANK genes code for a family of scaffolding proteins located in the postsynaptic density of excitatory synapses. To test the hypothesis that a mutation in SHANK1 contributes to the symptoms of autism, we evaluated Shank1(-/-) null mutant mice for behavioral phenotypes with relevance to autism, focusing on social communication. Ultrasonic vocalizations and the deposition of scent marks appear to be two major modes of mouse communication. Our findings revealed evidence for low levels of ultrasonic vocalizations and scent marks in Shank1(-/-) mice as compared to wildtype Shank1(+/+) littermate controls. Shank1(-/-) pups emitted fewer vocalizations than Shank1(+/+) pups when isolated from mother and littermates. In adulthood, genotype affected scent marking behavior in the presence of female urinary pheromones. Adult Shank1(-/-) males deposited fewer scent marks in proximity to female urine than Shank1(+/+) males. Call emission in response to female urinary pheromones also differed between genotypes. Shank1(+/+) mice changed their calling pattern dependent on previous female interactions, while Shank1(-/-) mice were unaffected, indicating a failure of Shank1(-/-) males to learn from a social experience. The reduced levels of ultrasonic vocalizations and scent marking behavior in Shank1(-/-) mice are consistent with a phenotype relevant to social communication deficits in autism.Markus WöhrFlorence I RoulletAlbert Y HungMorgan ShengJacqueline N CrawleyPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 6, p e20631 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Markus Wöhr
Florence I Roullet
Albert Y Hung
Morgan Sheng
Jacqueline N Crawley
Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
description Autism is a neurodevelopmental disorder with a strong genetic component. Core symptoms are abnormal reciprocal social interactions, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior with restricted interests. Candidate genes for autism include the SHANK gene family, as mutations in SHANK2 and SHANK3 have been detected in several autistic individuals. SHANK genes code for a family of scaffolding proteins located in the postsynaptic density of excitatory synapses. To test the hypothesis that a mutation in SHANK1 contributes to the symptoms of autism, we evaluated Shank1(-/-) null mutant mice for behavioral phenotypes with relevance to autism, focusing on social communication. Ultrasonic vocalizations and the deposition of scent marks appear to be two major modes of mouse communication. Our findings revealed evidence for low levels of ultrasonic vocalizations and scent marks in Shank1(-/-) mice as compared to wildtype Shank1(+/+) littermate controls. Shank1(-/-) pups emitted fewer vocalizations than Shank1(+/+) pups when isolated from mother and littermates. In adulthood, genotype affected scent marking behavior in the presence of female urinary pheromones. Adult Shank1(-/-) males deposited fewer scent marks in proximity to female urine than Shank1(+/+) males. Call emission in response to female urinary pheromones also differed between genotypes. Shank1(+/+) mice changed their calling pattern dependent on previous female interactions, while Shank1(-/-) mice were unaffected, indicating a failure of Shank1(-/-) males to learn from a social experience. The reduced levels of ultrasonic vocalizations and scent marking behavior in Shank1(-/-) mice are consistent with a phenotype relevant to social communication deficits in autism.
format article
author Markus Wöhr
Florence I Roullet
Albert Y Hung
Morgan Sheng
Jacqueline N Crawley
author_facet Markus Wöhr
Florence I Roullet
Albert Y Hung
Morgan Sheng
Jacqueline N Crawley
author_sort Markus Wöhr
title Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
title_short Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
title_full Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
title_fullStr Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
title_full_unstemmed Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
title_sort communication impairments in mice lacking shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/4059565f040041e597f0906290f714dd
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