Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction

Glutamate neurotransmission: A weakness for omega-3 Depletion of omega-3 fatty acids in a mouse model of schizophrenia with altered glutamate transmission has a lethal effect in males. Previous studies have suggested that omega-3 supplements may improve the symptoms of schizophrenia. Amy Ramsey and...

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Autores principales:	Rehnuma Islam, Marc-Olivier Trépanier, Marija Milenkovic, Wendy Horsfall, Ali Salahpour, Richard P. Bazinet, Amy J. Ramsey
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Psychiatry RC435-571
Acceso en línea:	https://doaj.org/article/cb4d223a6c6e4da884ca01d7933a7b64
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spelling	oai:doaj.org-article:cb4d223a6c6e4da884ca01d7933a7b642021-12-02T11:51:10ZVulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction10.1038/s41537-017-0014-82334-265Xhttps://doaj.org/article/cb4d223a6c6e4da884ca01d7933a7b642017-03-01T00:00:00Zhttps://doi.org/10.1038/s41537-017-0014-8https://doaj.org/toc/2334-265XGlutamate neurotransmission: A weakness for omega-3 Depletion of omega-3 fatty acids in a mouse model of schizophrenia with altered glutamate transmission has a lethal effect in males. Previous studies have suggested that omega-3 supplements may improve the symptoms of schizophrenia. Amy Ramsey and colleagues at the University of Toronto, Canada, show in an established genetic mouse model of the disease that omega-3 dietary supplementation increased brain omega-3 levels, but did not have any beneficial effects on features that mirror symptoms of patients with schizophrenia such as increased locomotor activity or reduced social behavior. Interestingly, omega-3 dietary depletion worsened the cognitive performance and drastically increased the mortality rate of male mutant mice. The mechanisms responsible for these effects remain to be determined, but the findings highlight a potentially serious vulnerability of patients to dietary omega-3 deficits.Rehnuma IslamMarc-Olivier TrépanierMarija MilenkovicWendy HorsfallAli SalahpourRichard P. BazinetAmy J. RamseyNature PortfolioarticlePsychiatryRC435-571ENnpj Schizophrenia, Vol 3, Iss 1, Pp 1-8 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Psychiatry RC435-571
spellingShingle	Psychiatry RC435-571 Rehnuma Islam Marc-Olivier Trépanier Marija Milenkovic Wendy Horsfall Ali Salahpour Richard P. Bazinet Amy J. Ramsey Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction
description	Glutamate neurotransmission: A weakness for omega-3 Depletion of omega-3 fatty acids in a mouse model of schizophrenia with altered glutamate transmission has a lethal effect in males. Previous studies have suggested that omega-3 supplements may improve the symptoms of schizophrenia. Amy Ramsey and colleagues at the University of Toronto, Canada, show in an established genetic mouse model of the disease that omega-3 dietary supplementation increased brain omega-3 levels, but did not have any beneficial effects on features that mirror symptoms of patients with schizophrenia such as increased locomotor activity or reduced social behavior. Interestingly, omega-3 dietary depletion worsened the cognitive performance and drastically increased the mortality rate of male mutant mice. The mechanisms responsible for these effects remain to be determined, but the findings highlight a potentially serious vulnerability of patients to dietary omega-3 deficits.
format	article
author	Rehnuma Islam Marc-Olivier Trépanier Marija Milenkovic Wendy Horsfall Ali Salahpour Richard P. Bazinet Amy J. Ramsey
author_facet	Rehnuma Islam Marc-Olivier Trépanier Marija Milenkovic Wendy Horsfall Ali Salahpour Richard P. Bazinet Amy J. Ramsey
author_sort	Rehnuma Islam
title	Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction
title_short	Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction
title_full	Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction
title_fullStr	Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction
title_full_unstemmed	Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction
title_sort	vulnerability to omega-3 deprivation in a mouse model of nmda receptor hypofunction
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/cb4d223a6c6e4da884ca01d7933a7b64
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Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction

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