Plastic nanoparticles interfere with extracellular vesicle pathway in primary astrocytes.

The extensive production and use of plastics in recent decades has led to environmental pollution. It has been discovered that plastic microparticles (MPs) and nanoparticles (NPs), formed under the influence of physical forces, can pose a significant health risk. Increasing evidence indicates that NPs can have various toxic effects, including oxidative stress and cell death.

Involvement of the Kinin B1 Receptor in Increased Permeability of Cerebral Microvessels in Rats Subjected to Autoimmune Encephalomyelitis.

Kinins are vasoactive peptides that are involved in various cellular mechanisms, including the inflammatory response. Kinins, released in vessel walls, exacerbate inflammation by modulating the production and release of pro-inflammatory factors via two types of G protein-related receptors-B1 and B2 receptors. B1 R is overexpressed during the inflammation that accompanies numerous neurological disorders, including multiple sclerosis (MS), in which loss of BBB integrity is an early pathomechanism of the disease.

Proinflammatory microglial response is a common mechanism of Aroclor 1254- and Tetrabromobisphenol-A-induced neurotoxicity in immature chronically exposed rats.

Polychlorinated biphenyls (PCBs) and brominated flame retardants (BFRs) are dominant environmental and food contaminants. Tetrabromobisphenol A (TBBPA) is the most widely used BFR in the world to improve the fire safety of laminates in electrical and electronic equipment. Aroclor 1254, one of the PCBs, is widely distributed in the environment due to its extensive use in industrial applications around the world.

Memantine Improves the Disturbed Glutamine and γ-Amino Butyric Acid Homeostasis in the Brain of Rats Subjected to Experimental Autoimmune Encephalomyelitis.

Glutamine (Gln), glutamate (Glu), and γ-amino butyric acid (GABA) are essential amino acids for brain metabolism and function. Astrocyte-derived Gln is the precursor for the two most important neurotransmitters in the central nervous system (CNS), which are the excitatory neurotransmitter Glu and the inhibitory neurotransmitter GABA. In addition to their roles in neurotransmission, these amino acids can be used as alternative substrates in brain metabolism that enable metabolic coupling between astrocytes and neurons in the glutamate-glutamine cycle (GGC).

Mutant Tau protein-induced abnormalities in the Na-dependent glutamine translocation and recycling and their impact on astrocyte-neuron integrity in vitro.

Tau-dependent neurodegeneration is accompanied by astrocytosis in a mouse trans-genic model, which replicates the neuropathological characteristic of tauopathy and other human neurodegenerative disorders where astrocyte activation precedes neuronal loss and is associated with disease progression. This indicates an important role of astrocytes in the development of the disease. Astrocytes derived from a transgenic mouse model expressing human Tau, exhibit changes in cellular markers of astrocyte neuroprotective function related to the glutamate-glutamine cycle (GGC), representing a key part of astrocyte-neuron integrity.