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Reduced acute nociception and chronic pain in Shank2(−/−) mice
Autism spectrum disorder is a debilitating mental illness and social issue. Autism spectrum disorder patients suffer from social isolation, cognitive deficits, compulsive behavior, and sensory deficits, including hyposensitivity to pain. However, recent studies argued that autism spectrum disorder p...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4956181/ https://www.ncbi.nlm.nih.gov/pubmed/27145803 http://dx.doi.org/10.1177/1744806916647056 |
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author | Ko, Hyoung-Gon Oh, Seog-Bae Zhuo, Min Kaang, Bong-Kiun |
author_facet | Ko, Hyoung-Gon Oh, Seog-Bae Zhuo, Min Kaang, Bong-Kiun |
author_sort | Ko, Hyoung-Gon |
collection | PubMed |
description | Autism spectrum disorder is a debilitating mental illness and social issue. Autism spectrum disorder patients suffer from social isolation, cognitive deficits, compulsive behavior, and sensory deficits, including hyposensitivity to pain. However, recent studies argued that autism spectrum disorder patients show physiological pain response and, in some cases, even extremely intense pain response to harmless stimulation. Recently, Shank gene family was reported as one of the genetic risk factors of autism spectrum disorder. Thus, in this study, we used Shank2(−)(/)(−) (Shank2 knock-out, KO) mice to investigate the controversial pain sensitivity issue and found that Shank2 KO mice showed reduced tactile perception and analgesia to chronic pain. |
format | Online Article Text |
id | pubmed-4956181 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-49561812016-08-12 Reduced acute nociception and chronic pain in Shank2(−/−) mice Ko, Hyoung-Gon Oh, Seog-Bae Zhuo, Min Kaang, Bong-Kiun Mol Pain Short Report Autism spectrum disorder is a debilitating mental illness and social issue. Autism spectrum disorder patients suffer from social isolation, cognitive deficits, compulsive behavior, and sensory deficits, including hyposensitivity to pain. However, recent studies argued that autism spectrum disorder patients show physiological pain response and, in some cases, even extremely intense pain response to harmless stimulation. Recently, Shank gene family was reported as one of the genetic risk factors of autism spectrum disorder. Thus, in this study, we used Shank2(−)(/)(−) (Shank2 knock-out, KO) mice to investigate the controversial pain sensitivity issue and found that Shank2 KO mice showed reduced tactile perception and analgesia to chronic pain. SAGE Publications 2016-05-04 /pmc/articles/PMC4956181/ /pubmed/27145803 http://dx.doi.org/10.1177/1744806916647056 Text en © The Author(s) 2016 http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Short Report Ko, Hyoung-Gon Oh, Seog-Bae Zhuo, Min Kaang, Bong-Kiun Reduced acute nociception and chronic pain in Shank2(−/−) mice |
title | Reduced acute nociception and chronic pain in Shank2(−/−) mice |
title_full | Reduced acute nociception and chronic pain in Shank2(−/−) mice |
title_fullStr | Reduced acute nociception and chronic pain in Shank2(−/−) mice |
title_full_unstemmed | Reduced acute nociception and chronic pain in Shank2(−/−) mice |
title_short | Reduced acute nociception and chronic pain in Shank2(−/−) mice |
title_sort | reduced acute nociception and chronic pain in shank2(−/−) mice |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4956181/ https://www.ncbi.nlm.nih.gov/pubmed/27145803 http://dx.doi.org/10.1177/1744806916647056 |
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