Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration

Abstract Mild blast traumatic brain injury (B-TBI) induced lasting cognitive impairments in novel object recognition and less severe deficits in Y-maze behaviors. B-TBI significantly reduced the levels of synaptophysin (SYP) protein staining in cortical (CTX) and hippocampal (HIPP) tissues. Treatmen...

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Autores principales:	Lital Rachmany, David Tweedie, Vardit Rubovitch, Yazhou Li, Harold W. Holloway, Dong Seok Kim, Whitney A. Ratliff, Jessica N. Saykally, Bruce A. Citron, Barry J. Hoffer, Nigel H. Greig, Chaim G. Pick
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ba14dd0658e44105ac602a7fca068d44
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spelling	oai:doaj.org-article:ba14dd0658e44105ac602a7fca068d442021-12-02T16:06:22ZExendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration10.1038/s41598-017-03792-92045-2322https://doaj.org/article/ba14dd0658e44105ac602a7fca068d442017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03792-9https://doaj.org/toc/2045-2322Abstract Mild blast traumatic brain injury (B-TBI) induced lasting cognitive impairments in novel object recognition and less severe deficits in Y-maze behaviors. B-TBI significantly reduced the levels of synaptophysin (SYP) protein staining in cortical (CTX) and hippocampal (HIPP) tissues. Treatment with exendin-4 (Ex-4) delivered by subcutaneous micro-osmotic pumps 48 hours prior to or 2 hours immediately after B-TBI prevented the induction of both cognitive deficits and B-TBI induced changes in SYP staining. The effects of a series of biaxial stretch injuries (BSI) on a neuronal derived cell line, HT22 cells, were assessed in an in vitro model of TBI. Biaxial stretch damage induced shrunken neurites and cell death. Treatment of HT22 cultures with Ex-4 (25 to 100 nM), prior to injury, attenuated the cytotoxic effects of BSI and preserved neurite length similar to sham treated cells. These data imply that treatment with Ex-4 may represent a viable option for the management of secondary events triggered by blast-induced, mild traumatic brain injury that is commonly observed in militarized zones.Lital RachmanyDavid TweedieVardit RubovitchYazhou LiHarold W. HollowayDong Seok KimWhitney A. RatliffJessica N. SaykallyBruce A. CitronBarry J. HofferNigel H. GreigChaim G. PickNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lital Rachmany David Tweedie Vardit Rubovitch Yazhou Li Harold W. Holloway Dong Seok Kim Whitney A. Ratliff Jessica N. Saykally Bruce A. Citron Barry J. Hoffer Nigel H. Greig Chaim G. Pick Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration
description	Abstract Mild blast traumatic brain injury (B-TBI) induced lasting cognitive impairments in novel object recognition and less severe deficits in Y-maze behaviors. B-TBI significantly reduced the levels of synaptophysin (SYP) protein staining in cortical (CTX) and hippocampal (HIPP) tissues. Treatment with exendin-4 (Ex-4) delivered by subcutaneous micro-osmotic pumps 48 hours prior to or 2 hours immediately after B-TBI prevented the induction of both cognitive deficits and B-TBI induced changes in SYP staining. The effects of a series of biaxial stretch injuries (BSI) on a neuronal derived cell line, HT22 cells, were assessed in an in vitro model of TBI. Biaxial stretch damage induced shrunken neurites and cell death. Treatment of HT22 cultures with Ex-4 (25 to 100 nM), prior to injury, attenuated the cytotoxic effects of BSI and preserved neurite length similar to sham treated cells. These data imply that treatment with Ex-4 may represent a viable option for the management of secondary events triggered by blast-induced, mild traumatic brain injury that is commonly observed in militarized zones.
format	article
author	Lital Rachmany David Tweedie Vardit Rubovitch Yazhou Li Harold W. Holloway Dong Seok Kim Whitney A. Ratliff Jessica N. Saykally Bruce A. Citron Barry J. Hoffer Nigel H. Greig Chaim G. Pick
author_facet	Lital Rachmany David Tweedie Vardit Rubovitch Yazhou Li Harold W. Holloway Dong Seok Kim Whitney A. Ratliff Jessica N. Saykally Bruce A. Citron Barry J. Hoffer Nigel H. Greig Chaim G. Pick
author_sort	Lital Rachmany
title	Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration
title_short	Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration
title_full	Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration
title_fullStr	Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration
title_full_unstemmed	Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration
title_sort	exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro tbi-induced hippocampal cellular degeneration
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/ba14dd0658e44105ac602a7fca068d44
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Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration

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