Utilize este identificador para referenciar este registo:
https://hdl.handle.net/1822/78349
Título: | Neuron-microglia contact-dependent mechanisms attenuate methamphetamine-induced microglia reactivity and enhance neuronal plasticity |
Autor(es): | 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 |
Palavras-chave: | Methamphetamine Neuron-to-microglia Neuroprotection Contact-dependent CD200 PSD95 |
Data: | 21-Jan-2022 |
Editora: | Multidisciplinary Digital Publishing Institute (MDPI) |
Revista: | Cells |
Citação: | Bravo, J.; Ribeiro, I.; Terceiro, A.F.; Andrade, E.B.; Portugal, C.C.; Lopes, I.M.; Azevedo, M.M.; Sousa, M.; Lopes, C.D.F.; Lobo, A.C.; Canedo, T.; Relvas, J.B.; Summavielle, T. Neuron–Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity. Cells 2022, 11, 355. https://doi.org/10.3390/cells11030355 |
Resumo(s): | 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. |
Tipo: | Artigo |
URI: | https://hdl.handle.net/1822/78349 |
DOI: | 10.3390/cells11030355 |
e-ISSN: | 2073-4409 |
Versão da editora: | https://www.mdpi.com/2073-4409/11/3/355 |
Arbitragem científica: | yes |
Acesso: | Acesso aberto |
Aparece nas coleções: |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
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cells-11-00355-v2.pdf | 22,06 MB | Adobe PDF | Ver/Abrir |
Este trabalho está licenciado sob uma Licença Creative Commons