Abstract
BackgroundMicroglia are important myeloid cells present in the brain parenchyma that serve a surveillance function in the central nervous system. Microglial cell activation results in neuroinflammation that, when prolonged, can disrupt immune homeostasis and neurogenesis. Activated microglia-derived extracellular vesicles (EVs) may be involved in the propagation of inflammatory responses and modulation of cell-to-cell communication. However, a complete understanding of how EVs are regulated by drugs of abuse, such as cocaine, is still lacking.FindingsCocaine exposure reduced human microglial cell (HMC3) viability, decreased expression of CD63 and dectin-1 in HMC3-derived EVs, and increased expression of the apoptotic marker histone H2A.x in HMC3-derived EVs.ConclusionCocaine impacts HMC3 cell viability and specific EV protein expression, which could disrupt cellular signaling and cell-to-cell communication.
Highlights
Microglial activation is a pivotal focus of neurobiology (Franco and Fernandez-Suarez, 2015; Liddelow et al, 2017; Regen et al, 2017)
HMC3 cells, an immortalized human microglial cell line, were exposed to 1 or 100 μM cocaine, which was freshly prepared in exosome-depleted medium from 5.9 mM stock, for 24 h
Cell viability, assessed using trypan blue exclusion assay, showed a significant decrease in cell viability after exposure to 1 or 100 μM cocaine compared with the control condition (Figure 1A and Supplementary Figures 1A, 5), indicating that cocaine has a detrimental effect on microglia cells
Summary
Microglial activation is a pivotal focus of neurobiology (Franco and Fernandez-Suarez, 2015; Liddelow et al, 2017; Regen et al, 2017). Microglia can be neuroprotective by mediating neuroinflammation and the release of various substrates (Polazzi and Monti, 2010; Chen and Trapp, 2016; Condello et al, 2018). This changes under various conditions (Szepesi et al, 2018). Microglia can release trophic factors which was evident when microglia were depleted with subsequent neuronal loss It appears that the pathological state may dictate whether the microglia is protective or not (Szepesi et al, 2018). A complete understanding of how EVs are regulated by drugs of abuse, such as cocaine, is still lacking
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