MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide

Autores
Capani, Francisco; Udovin, Lucas; Kobiec, Tamara; Menéndez Maissonave, Camila Belen; Toro Urrego, Nicolas; Kusnier, Carlos Federico; Otero-losada, Matilde Estela; Herrera, María Inés
Año de publicación
2021
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Statement of the Problem: Diminish in the oxygen levels prompted short and long-term alterations insynapses and related structures that are related to neuronal dysfunction and death. Perinatal asphyxia (PA) isan obstetric complication produced by an impaired gas exchange that lead to neonatal mortality and is adeterminant factor for neurodevelopmental disorders (1,2). Cumulative experimental evidence refersPalmitoylethanolamide (PEA) exerts neuroprotective actions in different models of brain injury andneurodegeneration (3) . Accordingly, we have observed PEA treatment could ameliorate hippocampal deficitin microtubule associated protein-2 (MAP-2) 1 month after PA. Therefore, the aim of the present study was toassess earlier neuroprotective effects of this endogenous compound using correlative light and electronmicroscopy.Methodology & Theoretical Orientation PA was induced by placing newborn Sprague Dawley rats in a 37° C water bath for 19 minutes. PEA treatment (10 mg/kg) was administered subcutaneously during the firsthour of life. Hippocampal modifications were analyzed by Immunohistochemistry and electron microscopy atpostnatal day 21 (P21), once the animals had completed synapse formation and reflex maturation. In CA1region, a decrease in MAP-2 reactive area was observed at P21 as a consequence of PA. In this way, MAP-2appears as an early biomarker of PA-induced hippocampal damage (Fig 1). In addition, subcelularmodifications were observed using electron microscopy techniques. After PA, neuronal cell body showed clearsigns such as nuclear fragmentation, dark cytoplasm and vesicles accumulation. PEA reverted thesemodifications.Conclusion & Significance Therefore, PEA treatment could attenuate this hippocampal dendritic dysfunction,representing a putative neuroprotective agent for the developing injured brain. Future studies on long-termMAP-2 modifications might help determine the efficacy of PEA treatment on PA-induced dendriticcytoskeletal derangements.
Fil: Capani, Francisco. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Udovin, Lucas. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kobiec, Tamara. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Menéndez Maissonave, Camila Belen. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
Fil: Toro Urrego, Nicolas. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kusnier, Carlos Federico. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Otero-losada, Matilde Estela. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Herrera, María Inés. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
Materia
PERINATAL ASPHYXIA
MAP-2
CA1 REGION
PALMITOYLETHANOLAMIDE
NEUROPROTECTION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/165963
Acceder
id CONICETDig_0fd974c2b4a3be2d8ca211731297a4a4
oai_identifier_str oai:ri.conicet.gov.ar:11336/165963
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of PalmitoylethanolamideCapani, FranciscoUdovin, LucasKobiec, TamaraMenéndez Maissonave, Camila BelenToro Urrego, NicolasKusnier, Carlos FedericoOtero-losada, Matilde EstelaHerrera, María InésPERINATAL ASPHYXIAMAP-2CA1 REGIONPALMITOYLETHANOLAMIDENEUROPROTECTIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Statement of the Problem: Diminish in the oxygen levels prompted short and long-term alterations insynapses and related structures that are related to neuronal dysfunction and death. Perinatal asphyxia (PA) isan obstetric complication produced by an impaired gas exchange that lead to neonatal mortality and is adeterminant factor for neurodevelopmental disorders (1,2). Cumulative experimental evidence refersPalmitoylethanolamide (PEA) exerts neuroprotective actions in different models of brain injury andneurodegeneration (3) . Accordingly, we have observed PEA treatment could ameliorate hippocampal deficitin microtubule associated protein-2 (MAP-2) 1 month after PA. Therefore, the aim of the present study was toassess earlier neuroprotective effects of this endogenous compound using correlative light and electronmicroscopy.Methodology & Theoretical Orientation PA was induced by placing newborn Sprague Dawley rats in a 37° C water bath for 19 minutes. PEA treatment (10 mg/kg) was administered subcutaneously during the firsthour of life. Hippocampal modifications were analyzed by Immunohistochemistry and electron microscopy atpostnatal day 21 (P21), once the animals had completed synapse formation and reflex maturation. In CA1region, a decrease in MAP-2 reactive area was observed at P21 as a consequence of PA. In this way, MAP-2appears as an early biomarker of PA-induced hippocampal damage (Fig 1). In addition, subcelularmodifications were observed using electron microscopy techniques. After PA, neuronal cell body showed clearsigns such as nuclear fragmentation, dark cytoplasm and vesicles accumulation. PEA reverted thesemodifications.Conclusion & Significance Therefore, PEA treatment could attenuate this hippocampal dendritic dysfunction,representing a putative neuroprotective agent for the developing injured brain. Future studies on long-termMAP-2 modifications might help determine the efficacy of PEA treatment on PA-induced dendriticcytoskeletal derangements.Fil: Capani, Francisco. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Udovin, Lucas. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Kobiec, Tamara. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Menéndez Maissonave, Camila Belen. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; ArgentinaFil: Toro Urrego, Nicolas. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Kusnier, Carlos Federico. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Otero-losada, Matilde Estela. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Herrera, María Inés. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; ArgentinaCambridge University Press2021-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/165963Capani, Francisco; Udovin, Lucas; Kobiec, Tamara; Menéndez Maissonave, Camila Belen; Toro Urrego, Nicolas; et al.; MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide; Cambridge University Press; Microscopy & Microanalysis; 27; 1; 6-2021; 1-21431-9276CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.cambridge.org/core/services/aop-cambridge-core/content/view/8CB14D6F752A2C8E14B6FEA844C459FC/S1431927621004281a.pdf/map-2-as-an-early-marker-of-hippocampal-damage-after-perinatal-asphyxia-and-neuroprotective-properties-of-palmitoylethanolamideinfo:eu-repo/semantics/altIdentifier/doi/10.1017/S1431927621004281info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:55:44Zoai:ri.conicet.gov.ar:11336/165963instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:55:45.079CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
title MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
spellingShingle MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
Capani, Francisco
PERINATAL ASPHYXIA
MAP-2
CA1 REGION
PALMITOYLETHANOLAMIDE
NEUROPROTECTION
title_short MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
title_full MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
title_fullStr MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
title_full_unstemmed MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
title_sort MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide
dc.creator.none.fl_str_mv Capani, Francisco
Udovin, Lucas
Kobiec, Tamara
Menéndez Maissonave, Camila Belen
Toro Urrego, Nicolas
Kusnier, Carlos Federico
Otero-losada, Matilde Estela
Herrera, María Inés
author Capani, Francisco
author_facet Capani, Francisco
Udovin, Lucas
Kobiec, Tamara
Menéndez Maissonave, Camila Belen
Toro Urrego, Nicolas
Kusnier, Carlos Federico
Otero-losada, Matilde Estela
Herrera, María Inés
author_role author
author2 Udovin, Lucas
Kobiec, Tamara
Menéndez Maissonave, Camila Belen
Toro Urrego, Nicolas
Kusnier, Carlos Federico
Otero-losada, Matilde Estela
Herrera, María Inés
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv PERINATAL ASPHYXIA
MAP-2
CA1 REGION
PALMITOYLETHANOLAMIDE
NEUROPROTECTION
topic PERINATAL ASPHYXIA
MAP-2
CA1 REGION
PALMITOYLETHANOLAMIDE
NEUROPROTECTION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Statement of the Problem: Diminish in the oxygen levels prompted short and long-term alterations insynapses and related structures that are related to neuronal dysfunction and death. Perinatal asphyxia (PA) isan obstetric complication produced by an impaired gas exchange that lead to neonatal mortality and is adeterminant factor for neurodevelopmental disorders (1,2). Cumulative experimental evidence refersPalmitoylethanolamide (PEA) exerts neuroprotective actions in different models of brain injury andneurodegeneration (3) . Accordingly, we have observed PEA treatment could ameliorate hippocampal deficitin microtubule associated protein-2 (MAP-2) 1 month after PA. Therefore, the aim of the present study was toassess earlier neuroprotective effects of this endogenous compound using correlative light and electronmicroscopy.Methodology & Theoretical Orientation PA was induced by placing newborn Sprague Dawley rats in a 37° C water bath for 19 minutes. PEA treatment (10 mg/kg) was administered subcutaneously during the firsthour of life. Hippocampal modifications were analyzed by Immunohistochemistry and electron microscopy atpostnatal day 21 (P21), once the animals had completed synapse formation and reflex maturation. In CA1region, a decrease in MAP-2 reactive area was observed at P21 as a consequence of PA. In this way, MAP-2appears as an early biomarker of PA-induced hippocampal damage (Fig 1). In addition, subcelularmodifications were observed using electron microscopy techniques. After PA, neuronal cell body showed clearsigns such as nuclear fragmentation, dark cytoplasm and vesicles accumulation. PEA reverted thesemodifications.Conclusion & Significance Therefore, PEA treatment could attenuate this hippocampal dendritic dysfunction,representing a putative neuroprotective agent for the developing injured brain. Future studies on long-termMAP-2 modifications might help determine the efficacy of PEA treatment on PA-induced dendriticcytoskeletal derangements.
Fil: Capani, Francisco. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Udovin, Lucas. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kobiec, Tamara. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Menéndez Maissonave, Camila Belen. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
Fil: Toro Urrego, Nicolas. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kusnier, Carlos Federico. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Otero-losada, Matilde Estela. Universidad Abierta Interamericana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Herrera, María Inés. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
description Statement of the Problem: Diminish in the oxygen levels prompted short and long-term alterations insynapses and related structures that are related to neuronal dysfunction and death. Perinatal asphyxia (PA) isan obstetric complication produced by an impaired gas exchange that lead to neonatal mortality and is adeterminant factor for neurodevelopmental disorders (1,2). Cumulative experimental evidence refersPalmitoylethanolamide (PEA) exerts neuroprotective actions in different models of brain injury andneurodegeneration (3) . Accordingly, we have observed PEA treatment could ameliorate hippocampal deficitin microtubule associated protein-2 (MAP-2) 1 month after PA. Therefore, the aim of the present study was toassess earlier neuroprotective effects of this endogenous compound using correlative light and electronmicroscopy.Methodology & Theoretical Orientation PA was induced by placing newborn Sprague Dawley rats in a 37° C water bath for 19 minutes. PEA treatment (10 mg/kg) was administered subcutaneously during the firsthour of life. Hippocampal modifications were analyzed by Immunohistochemistry and electron microscopy atpostnatal day 21 (P21), once the animals had completed synapse formation and reflex maturation. In CA1region, a decrease in MAP-2 reactive area was observed at P21 as a consequence of PA. In this way, MAP-2appears as an early biomarker of PA-induced hippocampal damage (Fig 1). In addition, subcelularmodifications were observed using electron microscopy techniques. After PA, neuronal cell body showed clearsigns such as nuclear fragmentation, dark cytoplasm and vesicles accumulation. PEA reverted thesemodifications.Conclusion & Significance Therefore, PEA treatment could attenuate this hippocampal dendritic dysfunction,representing a putative neuroprotective agent for the developing injured brain. Future studies on long-termMAP-2 modifications might help determine the efficacy of PEA treatment on PA-induced dendriticcytoskeletal derangements.
publishDate 2021
dc.date.none.fl_str_mv 2021-06
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/165963
Capani, Francisco; Udovin, Lucas; Kobiec, Tamara; Menéndez Maissonave, Camila Belen; Toro Urrego, Nicolas; et al.; MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide; Cambridge University Press; Microscopy & Microanalysis; 27; 1; 6-2021; 1-2
1431-9276
CONICET Digital
CONICET
url http://hdl.handle.net/11336/165963
identifier_str_mv Capani, Francisco; Udovin, Lucas; Kobiec, Tamara; Menéndez Maissonave, Camila Belen; Toro Urrego, Nicolas; et al.; MAP-2 as an early marker of hippocampal damage after perinatal asphyxia and neuroprotective properties of Palmitoylethanolamide; Cambridge University Press; Microscopy & Microanalysis; 27; 1; 6-2021; 1-2
1431-9276
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.cambridge.org/core/services/aop-cambridge-core/content/view/8CB14D6F752A2C8E14B6FEA844C459FC/S1431927621004281a.pdf/map-2-as-an-early-marker-of-hippocampal-damage-after-perinatal-asphyxia-and-neuroprotective-properties-of-palmitoylethanolamide
info:eu-repo/semantics/altIdentifier/doi/10.1017/S1431927621004281
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Cambridge University Press
publisher.none.fl_str_mv Cambridge University Press
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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