AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation

Autores
Cabrera Kreiker, Ricardo Jorge; Baiardi, Lucia; Bregonzio Diaz, Claudia
Año de publicación
2022
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: Amphetamines constitute a group of drugs associated with clinical use and illicit consumption. They induce dopamine neurotransmission and promote astrocyte reactivity and microglial activation events associated with their neurotoxic actions. The neuroinflammatory response induced by amphetamines occurs as a consequence of mechanisms that involve oxidative stress, glial reactivity and apoptosis. Brain angiotensin II, through its AT1 receptor (AT1-R), modulates dopaminergic, glutamatergic and GABAergic neurotransmission, which are involve in cognition, emotions and stress responses. AT1-R is present in neurons, astrocytes, microglia and endothelial cells having a key role in the development of an oxidative/inflammatory microenvironment. AT1-R promotes the initiation and progression of local brain inflammatory and oxidative responses under dopamine imbalance conditions. The available evidences support the protective effects of AT1-R blockade for the deleterious effects induced by amphetamine.Conclusion: The available evidences, together with the results obtained by our group, open the possibility to postulate AT1-R as a possible therapeutic target for neuroinflammatory responses associated with dopamine imbalanced related disorders.
Fil: Cabrera Kreiker, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Baiardi, Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina
Fil: Bregonzio Diaz, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina
Materia
ANGIOTENSIN
ATTENTION DEFICIT
PSYCHOSTIMULANTS
NEUROINFLAMMATION
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:11336/204544
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammationCabrera Kreiker, Ricardo JorgeBaiardi, LuciaBregonzio Diaz, ClaudiaANGIOTENSINATTENTION DEFICITPSYCHOSTIMULANTSNEUROINFLAMMATIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: Amphetamines constitute a group of drugs associated with clinical use and illicit consumption. They induce dopamine neurotransmission and promote astrocyte reactivity and microglial activation events associated with their neurotoxic actions. The neuroinflammatory response induced by amphetamines occurs as a consequence of mechanisms that involve oxidative stress, glial reactivity and apoptosis. Brain angiotensin II, through its AT1 receptor (AT1-R), modulates dopaminergic, glutamatergic and GABAergic neurotransmission, which are involve in cognition, emotions and stress responses. AT1-R is present in neurons, astrocytes, microglia and endothelial cells having a key role in the development of an oxidative/inflammatory microenvironment. AT1-R promotes the initiation and progression of local brain inflammatory and oxidative responses under dopamine imbalance conditions. The available evidences support the protective effects of AT1-R blockade for the deleterious effects induced by amphetamine.Conclusion: The available evidences, together with the results obtained by our group, open the possibility to postulate AT1-R as a possible therapeutic target for neuroinflammatory responses associated with dopamine imbalanced related disorders.Fil: Cabrera Kreiker, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Baiardi, Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Bregonzio Diaz, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaBentham Science Publishers2022-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/204544Cabrera Kreiker, Ricardo Jorge; Baiardi, Lucia; Bregonzio Diaz, Claudia; AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation; Bentham Science Publishers; Protein and Peptide Letters; 29; 5; 5-2022; 371-3740929-8665CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.2174/0929866529666220330154218info:eu-repo/semantics/altIdentifier/url/https://www.eurekaselect.com/article/122067info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:40:14Zoai:ri.conicet.gov.ar:11336/204544instacron: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:34982025-09-29 10:40:14.459CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
title AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
spellingShingle AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
Cabrera Kreiker, Ricardo Jorge
ANGIOTENSIN
ATTENTION DEFICIT
PSYCHOSTIMULANTS
NEUROINFLAMMATION
title_short AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
title_full AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
title_fullStr AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
title_full_unstemmed AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
title_sort AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation
dc.creator.none.fl_str_mv Cabrera Kreiker, Ricardo Jorge
Baiardi, Lucia
Bregonzio Diaz, Claudia
author Cabrera Kreiker, Ricardo Jorge
author_facet Cabrera Kreiker, Ricardo Jorge
Baiardi, Lucia
Bregonzio Diaz, Claudia
author_role author
author2 Baiardi, Lucia
Bregonzio Diaz, Claudia
author2_role author
author
dc.subject.none.fl_str_mv ANGIOTENSIN
ATTENTION DEFICIT
PSYCHOSTIMULANTS
NEUROINFLAMMATION
topic ANGIOTENSIN
ATTENTION DEFICIT
PSYCHOSTIMULANTS
NEUROINFLAMMATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background: Amphetamines constitute a group of drugs associated with clinical use and illicit consumption. They induce dopamine neurotransmission and promote astrocyte reactivity and microglial activation events associated with their neurotoxic actions. The neuroinflammatory response induced by amphetamines occurs as a consequence of mechanisms that involve oxidative stress, glial reactivity and apoptosis. Brain angiotensin II, through its AT1 receptor (AT1-R), modulates dopaminergic, glutamatergic and GABAergic neurotransmission, which are involve in cognition, emotions and stress responses. AT1-R is present in neurons, astrocytes, microglia and endothelial cells having a key role in the development of an oxidative/inflammatory microenvironment. AT1-R promotes the initiation and progression of local brain inflammatory and oxidative responses under dopamine imbalance conditions. The available evidences support the protective effects of AT1-R blockade for the deleterious effects induced by amphetamine.Conclusion: The available evidences, together with the results obtained by our group, open the possibility to postulate AT1-R as a possible therapeutic target for neuroinflammatory responses associated with dopamine imbalanced related disorders.
Fil: Cabrera Kreiker, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Baiardi, Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina
Fil: Bregonzio Diaz, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina
description Background: Amphetamines constitute a group of drugs associated with clinical use and illicit consumption. They induce dopamine neurotransmission and promote astrocyte reactivity and microglial activation events associated with their neurotoxic actions. The neuroinflammatory response induced by amphetamines occurs as a consequence of mechanisms that involve oxidative stress, glial reactivity and apoptosis. Brain angiotensin II, through its AT1 receptor (AT1-R), modulates dopaminergic, glutamatergic and GABAergic neurotransmission, which are involve in cognition, emotions and stress responses. AT1-R is present in neurons, astrocytes, microglia and endothelial cells having a key role in the development of an oxidative/inflammatory microenvironment. AT1-R promotes the initiation and progression of local brain inflammatory and oxidative responses under dopamine imbalance conditions. The available evidences support the protective effects of AT1-R blockade for the deleterious effects induced by amphetamine.Conclusion: The available evidences, together with the results obtained by our group, open the possibility to postulate AT1-R as a possible therapeutic target for neuroinflammatory responses associated with dopamine imbalanced related disorders.
publishDate 2022
dc.date.none.fl_str_mv 2022-05
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/11336/204544
Cabrera Kreiker, Ricardo Jorge; Baiardi, Lucia; Bregonzio Diaz, Claudia; AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation; Bentham Science Publishers; Protein and Peptide Letters; 29; 5; 5-2022; 371-374
0929-8665
CONICET Digital
CONICET
url http://hdl.handle.net/11336/204544
identifier_str_mv Cabrera Kreiker, Ricardo Jorge; Baiardi, Lucia; Bregonzio Diaz, Claudia; AT1 Receptor as a Potential Target in Amphetamine-induced Neuro-inflammation; Bentham Science Publishers; Protein and Peptide Letters; 29; 5; 5-2022; 371-374
0929-8665
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.2174/0929866529666220330154218
info:eu-repo/semantics/altIdentifier/url/https://www.eurekaselect.com/article/122067
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
application/pdf
dc.publisher.none.fl_str_mv Bentham Science Publishers
publisher.none.fl_str_mv Bentham Science Publishers
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
_version_ 1844614429956636672
score 13.070432

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