Microfluidic technology has become a valuable tool to the scientific community, allowing researchers to study fine cellular mechanisms with higher variable control compared with conventional systems. It has evolved tremendously, and its applicability and flexibility made its usage grow exponentially and transversely to several research fields. This has been particularly noticeable in neuroscience research, where microfluidic platforms made it possible to address specific questions extending from axonal guidance, synapse formation, or axonal transport to the development of 3D models of the CNS to allow pharmacological testing and drug screening. Furthermore, the continuous upgrade of microfluidic platforms has allowed a deeper study of the communication occurring between different neuronal and glial cells or between neurons and other peripheral tissues, both in physiological and pathological conditions. Importantly, the evolution of microfluidic technology has always been accompanied by the development of new computational tools addressing data acquisition, analysis, and modeling.

3,4-Methylenedioxymethamphetamine (MDMA)-induced neurotoxicity and the protective role of monoamine oxidase-B (MAO-B) inhibition were evaluated at the mitochondrial level in various regions of the adolescent rat brain. Four groups of adolescent male Wistar rats were used: (1) saline control, (2) exposed to MDMA (4 × 10 mg/kg, i.p.; two hourly), (3) treated with selegiline (2 mg/kg, i.p.) 30 min before the same dosing of MDMA, and (4) treated with selegiline (2 mg/kg, i.p.). Body temperatures were monitored throughout the whole experiment. Animals were killed 2 weeks later, and mitochondria were isolated from several brain regions. Our results showed that “binge” MDMA administration causes, along with sustained hyperthermia, long-term alterations in brain mitochondria as evidenced by increased levels of lipid peroxides and protein carbonyls. Additionally, analysis of mitochondrial DNA (mtDNA) revealed that NDI nicotinamide adenine dinucleotide phosphate dehydrogenase subunit I and NDII (nicotinamide adenine dinucleotide phosphate dehydrogenase subunit II) subunits of mitochondrial complex I and cytochromecoxidase subunit I of complex IV suffered deletions in MDMA-exposed animals. Inhibition of MAO-B by selegiline did not reduce hyperthermia but reversed MDMA-induced effects in the oxidative stress markers, mtDNA, and related protein expression. These results indicate that monoamine oxidation by MAO-B with subsequent mitochondrial damage may be an important contributing factor for MDMA-induced neurotoxicity.

Joint replacement surgery is the gold-standard therapeutic approach to treat patients with end-stage hip and knee arthritis, providing pain relief and joint function recovery. Despite the improvements in implant design and surgical techniques, revisions after total joint replacement are expected to grow. The periprosthetic inflammation, featured by the sustained inflammatory response to the implant debris, elicits the activation of osteoclasts and consequent periprosthetic osteolysis (PPOL), ultimately leading to implant aseptic loosening, which is the most common cause of long-term implant failure. There are currently no effective strategies to control periprosthetic inflammation, and long-term implant survival remains a major challenge in orthopedics. A broad knowledge of the mechanisms underlying the biological response to implant debris would support the development of novel and effective pharmacological strategies to manage PPOL and promote implant lifespan. In this review, a detailed description of the cellular and the molecular mechanisms underlying the biological response to implant debris is provided, highlighting the most recent findings. Furthermore, we reviewed novel therapeutic strategies that are being investigated to prevent inflammatory periprosthetic osteolysis.

We presented a microfluidic-based coculture system as a new tool to be explored for modeling biological processes and pharmacological screening concerning peripheral tissues innervation.