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Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity

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Resumo:Exposure to methamphetamine (Meth) has been classically associated with damage to neuronal terminals. However, it is now becoming clear that addiction may also result from the interplay between glial cells and neurons. Recently, we demonstrated that binge Meth administration promotes microgliosis and microglia pro-inflammation via astrocytic glutamate release in a TNF/IP<sub>3</sub>R2-Ca<sup>2+</sup>-dependent manner. Here, we investigated the contribution of neuronal cells to this process. As the crosstalk between microglia and neurons may occur by contact-dependent and/or contact-independent mechanisms, we developed co-cultures of primary neurons and microglia in microfluidic devices to investigate how their interaction affects Meth-induced microglia activation. Our results show that neurons exposed to Meth do not activate microglia in a cell-autonomous way but require astrocyte mediation. Importantly, we found that neurons can partially prevent Meth-induced microglia activation via astrocytes, which seems to be achieved by increasing arginase 1 expression and strengthening the CD200/CD200r pathway. We also observed an increase in synaptic individual area, as determined by co-localization of pre- and post-synaptic markers. The present study provides evidence that contact-dependent mechanisms between neurons and microglia can attenuate pro-inflammatory events such as Meth-induced microglia activation.
Autores principais:Bravo, Joana
Outros Autores:Ribeiro, Inês Moreira; Terceiro, Ana Filipa; Andrade, Elva B.; Portugal, Camila Cabral; Lopes, Igor M.; Azevedo, Maria M.; Sousa, Mafalda; Lopes, Cátia D. F.; Lobo, Andrea C.; Canedo, Teresa; Relvas, João Bettencourt; Summavielle, Teresa
Assunto:Methamphetamine Neuron-to-microglia Neuroprotection Contact-dependent CD200 PSD95
Ano:2022
País:Portugal
Tipo de documento:artigo
Tipo de acesso:acesso aberto
Instituição associada:Universidade do Minho
Idioma:inglês
Origem:RepositóriUM - Universidade do Minho
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author Bravo, Joana
author2 Ribeiro, Inês Moreira
Terceiro, Ana Filipa
Andrade, Elva B.
Portugal, Camila Cabral
Lopes, Igor M.
Azevedo, Maria M.
Sousa, Mafalda
Lopes, Cátia D. F.
Lobo, Andrea C.
Canedo, Teresa
Relvas, João Bettencourt
Summavielle, Teresa
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author_facet Bravo, Joana
Ribeiro, Inês Moreira
Terceiro, Ana Filipa
Andrade, Elva B.
Portugal, Camila Cabral
Lopes, Igor M.
Azevedo, Maria M.
Sousa, Mafalda
Lopes, Cátia D. F.
Lobo, Andrea C.
Canedo, Teresa
Relvas, João Bettencourt
Summavielle, Teresa
author_role author
contributor_name_str_mv Universidade do Minho
country_str PT
creators_json_txt [{\"Person.name\":\"Bravo, Joana\"},{\"Person.name\":\"Ribeiro, Inês Moreira\"},{\"Person.name\":\"Terceiro, Ana Filipa\"},{\"Person.name\":\"Andrade, Elva B.\"},{\"Person.name\":\"Portugal, Camila Cabral\"},{\"Person.name\":\"Lopes, Igor M.\"},{\"Person.name\":\"Azevedo, Maria M.\"},{\"Person.name\":\"Sousa, Mafalda\"},{\"Person.name\":\"Lopes, Cátia D. F.\"},{\"Person.name\":\"Lobo, Andrea C.\"},{\"Person.name\":\"Canedo, Teresa\"},{\"Person.name\":\"Relvas, João Bettencourt\"},{\"Person.name\":\"Summavielle, Teresa\"}]
datacite.contributors.contributor.contributorName.fl_str_mv Universidade do Minho
datacite.creators.creator.creatorName.fl_str_mv Bravo, Joana
Ribeiro, Inês Moreira
Terceiro, Ana Filipa
Andrade, Elva B.
Portugal, Camila Cabral
Lopes, Igor M.
Azevedo, Maria M.
Sousa, Mafalda
Lopes, Cátia D. F.
Lobo, Andrea C.
Canedo, Teresa
Relvas, João Bettencourt
Summavielle, Teresa
datacite.date.Accepted.fl_str_mv 2022-01-21T00:00:00Z
datacite.date.available.fl_str_mv 2022-06-13T09:18:02Z
datacite.date.embargoed.fl_str_mv 2022-06-13T09:18:02Z
datacite.rights.fl_str_mv http://purl.org/coar/access_right/c_abf2
datacite.subjects.subject.fl_str_mv Methamphetamine
Neuron-to-microglia
Neuroprotection
Contact-dependent
CD200
PSD95
datacite.titles.title.fl_str_mv Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
dc.contributor.none.fl_str_mv Universidade do Minho
dc.creator.none.fl_str_mv Bravo, Joana
Ribeiro, Inês Moreira
Terceiro, Ana Filipa
Andrade, Elva B.
Portugal, Camila Cabral
Lopes, Igor M.
Azevedo, Maria M.
Sousa, Mafalda
Lopes, Cátia D. F.
Lobo, Andrea C.
Canedo, Teresa
Relvas, João Bettencourt
Summavielle, Teresa
dc.date.Accepted.fl_str_mv 2022-01-21T00:00:00Z
dc.date.available.fl_str_mv 2022-06-13T09:18:02Z
dc.date.embargoed.fl_str_mv 2022-06-13T09:18:02Z
dc.format.none.fl_str_mv application/pdf
dc.identifier.none.fl_str_mv https://hdl.handle.net/1822/78349
dc.language.none.fl_str_mv eng
dc.publisher.none.fl_str_mv Multidisciplinary Digital Publishing Institute (MDPI)
dc.rights.cclincense.fl_str_mv http://creativecommons.org/licenses/by/4.0/
dc.rights.none.fl_str_mv http://purl.org/coar/access_right/c_abf2
dc.rights.rights.copyright.fl_str_mv openAccess
dc.subject.none.fl_str_mv Methamphetamine
Neuron-to-microglia
Neuroprotection
Contact-dependent
CD200
PSD95
dc.title.fl_str_mv Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
dc.type.none.fl_str_mv http://purl.org/coar/resource_type/c_6501
description Exposure to methamphetamine (Meth) has been classically associated with damage to neuronal terminals. However, it is now becoming clear that addiction may also result from the interplay between glial cells and neurons. Recently, we demonstrated that binge Meth administration promotes microgliosis and microglia pro-inflammation via astrocytic glutamate release in a TNF/IP<sub>3</sub>R2-Ca<sup>2+</sup>-dependent manner. Here, we investigated the contribution of neuronal cells to this process. As the crosstalk between microglia and neurons may occur by contact-dependent and/or contact-independent mechanisms, we developed co-cultures of primary neurons and microglia in microfluidic devices to investigate how their interaction affects Meth-induced microglia activation. Our results show that neurons exposed to Meth do not activate microglia in a cell-autonomous way but require astrocyte mediation. Importantly, we found that neurons can partially prevent Meth-induced microglia activation via astrocytes, which seems to be achieved by increasing arginase 1 expression and strengthening the CD200/CD200r pathway. We also observed an increase in synaptic individual area, as determined by co-localization of pre- and post-synaptic markers. The present study provides evidence that contact-dependent mechanisms between neurons and microglia can attenuate pro-inflammatory events such as Meth-induced microglia activation.
dirty 0
eu_rights_str_mv openAccess
format article
fulltext.url.fl_str_mv https://prod-dspace.uminho.pt/bitstreams/8f8dd91e-ce11-455c-bc0b-c4a25072df77/download
id rum_e71be0a4e580f30cd7259e2fd60f9239
identifier.url.fl_str_mv https://hdl.handle.net/1822/78349
instacron_str repositorium
institution Universidade do Minho
instname_str Universidade do Minho
language eng
network_acronym_str rum
network_name_str RepositóriUM - Universidade do Minho
oai_identifier_str oai:repositorium.uminho.pt:1822/78349
organization_str_mv urn:organizationAcronym:repositorium
person_str_mv Bravo, Joana
Ribeiro, Inês Moreira
Terceiro, Ana Filipa
Andrade, Elva B.
Portugal, Camila Cabral
Lopes, Igor M.
Azevedo, Maria M.
Sousa, Mafalda
Lopes, Cátia D. F.
Lobo, Andrea C.
Canedo, Teresa
Relvas, João Bettencourt
Summavielle, Teresa
publishDate 2022
publisher.none.fl_str_mv Multidisciplinary Digital Publishing Institute (MDPI)
reponame_str RepositóriUM - Universidade do Minho
repository_id_str urn:repositoryAcronym:rum
service_str_mv urn:repositoryAcronym:rum
spelling engMultidisciplinary Digital Publishing Institute (MDPI)porExposure to methamphetamine (Meth) has been classically associated with damage to neuronal terminals. However, it is now becoming clear that addiction may also result from the interplay between glial cells and neurons. Recently, we demonstrated that binge Meth administration promotes microgliosis and microglia pro-inflammation via astrocytic glutamate release in a TNF/IP<sub>3</sub>R2-Ca<sup>2+</sup>-dependent manner. Here, we investigated the contribution of neuronal cells to this process. As the crosstalk between microglia and neurons may occur by contact-dependent and/or contact-independent mechanisms, we developed co-cultures of primary neurons and microglia in microfluidic devices to investigate how their interaction affects Meth-induced microglia activation. Our results show that neurons exposed to Meth do not activate microglia in a cell-autonomous way but require astrocyte mediation. Importantly, we found that neurons can partially prevent Meth-induced microglia activation via astrocytes, which seems to be achieved by increasing arginase 1 expression and strengthening the CD200/CD200r pathway. We also observed an increase in synaptic individual area, as determined by co-localization of pre- and post-synaptic markers. The present study provides evidence that contact-dependent mechanisms between neurons and microglia can attenuate pro-inflammatory events such as Meth-induced microglia activation.application/pdfporNeuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticityBravo, JoanaRibeiro, Inês MoreiraTerceiro, Ana FilipaAndrade, Elva B.Portugal, Camila CabralLopes, Igor M.Azevedo, Maria M.Sousa, MafaldaLopes, Cátia D. F.Lobo, Andrea C.Canedo, TeresaRelvas, João BettencourtSummavielle, TeresaHostingInstitutionOrganizationalUniversidade do Minhoe-mailmailto:repositorium@usdb.uminho.ptrepositorium@usdb.uminho.ptDOIIsPartOf10.3390/cells110303552022-06-13T09:18:02Z2022-01-212022-02-11T14:46:27Z2022-01-21T00:00:00ZHandlehttps://hdl.handle.net/1822/78349http://purl.org/coar/access_right/c_abf2open accessMethamphetamineNeuron-to-microgliaNeuroprotectionContact-dependentCD200PSD9522594242 bytesliteraturehttp://purl.org/coar/resource_type/c_6501journal article2022-01-21http://creativecommons.org/licenses/by/4.0/openAccesshttp://purl.org/coar/access_right/c_abf2application/pdffulltexthttps://prod-dspace.uminho.pt/bitstreams/8f8dd91e-ce11-455c-bc0b-c4a25072df77/download
spellingShingle Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
Bravo, Joana
Methamphetamine
Neuron-to-microglia
Neuroprotection
Contact-dependent
CD200
PSD95
status SINGLETON
subject.fl_str_mv Methamphetamine
Neuron-to-microglia
Neuroprotection
Contact-dependent
CD200
PSD95
title Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
title_full Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
title_fullStr Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
title_full_unstemmed Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
title_short Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
title_sort Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity
topic Methamphetamine
Neuron-to-microglia
Neuroprotection
Contact-dependent
CD200
PSD95
topic_facet Methamphetamine
Neuron-to-microglia
Neuroprotection
Contact-dependent
CD200
PSD95
url https://hdl.handle.net/1822/78349
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