Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity
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 an...
| Autores: | , , , , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2022 |
| País: | España |
| Institución: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/184165 |
| Acceso en línea: | https://hdl.handle.net/2445/184165 |
| Access Level: | acceso abierto |
| Palabra clave: | Estimulants Neuròglia Stimulants Neuroglia |
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Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal PlasticityPortugal, Camila CabralBravo, JoanaRibeiro, InesTerceiro, Ana FilipaAndrade, Elva B.Lopes, Igor M.Azevedo, Maria M.Sousa, Mafalda Machado deLopes, Catia D. F.Lobo, Andrea C.Canedo, TeresaBettencourt Relvas, JoaoSummavielle, TeresaEstimulantsNeurògliaStimulantsNeurogliaExposure 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(3)R2-Ca2+-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.NLM (Medline)2022info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/184165Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC))reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.3390/cells11030355Cells, 2022, vol 11, num 3https://doi.org/10.3390/cells11030355cc by (c) Portugal, Camila Cabral et al., 2022http://creativecommons.org/licenses/by/3.0/es/info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1841652026-05-27T06:46:51Z |
| dc.title.none.fl_str_mv |
Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity |
| title |
Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity |
| spellingShingle |
Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity Portugal, Camila Cabral Estimulants Neuròglia Stimulants Neuroglia |
| title_short |
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_sort |
Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity |
| dc.creator.none.fl_str_mv |
Portugal, Camila Cabral Bravo, Joana Ribeiro, Ines Terceiro, Ana Filipa Andrade, Elva B. Lopes, Igor M. Azevedo, Maria M. Sousa, Mafalda Machado de Lopes, Catia D. F. Lobo, Andrea C. Canedo, Teresa Bettencourt Relvas, Joao Summavielle, Teresa |
| author |
Portugal, Camila Cabral |
| author_facet |
Portugal, Camila Cabral Bravo, Joana Ribeiro, Ines Terceiro, Ana Filipa Andrade, Elva B. Lopes, Igor M. Azevedo, Maria M. Sousa, Mafalda Machado de Lopes, Catia D. F. Lobo, Andrea C. Canedo, Teresa Bettencourt Relvas, Joao Summavielle, Teresa |
| author_role |
author |
| author2 |
Bravo, Joana Ribeiro, Ines Terceiro, Ana Filipa Andrade, Elva B. Lopes, Igor M. Azevedo, Maria M. Sousa, Mafalda Machado de Lopes, Catia D. F. Lobo, Andrea C. Canedo, Teresa Bettencourt Relvas, Joao Summavielle, Teresa |
| author2_role |
author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Estimulants Neuròglia Stimulants Neuroglia |
| topic |
Estimulants Neuròglia Stimulants Neuroglia |
| 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(3)R2-Ca2+-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. |
| publishDate |
2022 |
| dc.date.none.fl_str_mv |
2022 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
| format |
article |
| status_str |
publishedVersion |
| dc.identifier.none.fl_str_mv |
https://hdl.handle.net/2445/184165 |
| url |
https://hdl.handle.net/2445/184165 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
Reproducció del document publicat a: https://doi.org/10.3390/cells11030355 Cells, 2022, vol 11, num 3 https://doi.org/10.3390/cells11030355 |
| dc.rights.none.fl_str_mv |
cc by (c) Portugal, Camila Cabral et al., 2022 http://creativecommons.org/licenses/by/3.0/es/ info:eu-repo/semantics/openAccess |
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cc by (c) Portugal, Camila Cabral et al., 2022 http://creativecommons.org/licenses/by/3.0/es/ |
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openAccess |
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application/pdf |
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NLM (Medline) |
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NLM (Medline) |
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Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC)) reponame:Dipòsit Digital de la UB instname:Universidad de Barcelona |
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Universidad de Barcelona |
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Dipòsit Digital de la UB |
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Dipòsit Digital de la UB |
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