Neuron-Microglia Contact-Dependent Mechanisms Attenuate Methamphetamine-Induced Microglia Reactivity and Enhance Neuronal Plasticity

• Tipo: Artigo em Revista Científica Internacional
• Data: 2022

Autores

Bravo, J (Autor) Outra; Ribeiro, I (Autor) Outra; Terceiro, AF (Autor) Outra; Andrade, EB (Autor) Outra; Portugal, CC (Autor) Outra; Lopes, IM (Autor) Outra; Azevedo, MM (Autor) Outra; Sousa, M (Autor) Outra; Lopes, CDF (Autor) Outra; Lobo, AC (Autor) Outra; Canedo, T (Autor) Outra; Relvas, JB (Autor) FMUP; Summavielle, T (Autor) Outra

Revista

Título: Cells

Vol. 11

ISSN: 2073-4409

Editora: MDPI

Indexação

ISI Web of Knowledge - 0 Citações

Scopus - 0 Citações

Outras Informações

ID Authenticus: P-00W-624

DOI: 10.3390/cells11030355

Abstract (EN): 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.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 17