Perspectives in Intraoperative Diagnostics of Human Gliomas

Figure 1

Physiological comparison of normal and reactive astrocytes. (a) Normal astrocytes show a high level of expression of EAATs 1 and 2, which control the extracellular glutamate concentration around 25 nM. The cysteine-glutamate antiporters () provide the exchange of cysteine from the extracellular space on glutamine. Transformation of glutamate (Glu) to inactive form, glutamine (Gln), is carried out by glutamine synthase. The resting membrane potential in normal astrocytes holds around −90 mV; (b) the expression of EAAT1 in reactive astrocytes is significantly lower than in normal, whereas the EAAT2 type is absent which leads to the increase of extracellular glutamate concentration up to 1–100 μM. The cysteine-glutamate antiporters () in reactive astrocytes perform the exchange of cysteine from the extracellular space to glutamate which causes additional increase of extracellular glutamate concentration. Inside the astrocyte cystein (Cys) is converted to the glutation (GSH) and leads to the rise of resistance to oxidation. The resting membrane potential in reactive astrocytes equilibrates around −60 mV due to alterations in chloride homeostasis. Reactive astrocytes regulate their volume by releasing water through aquaporin channels (AQPR 1 and 2) and are characterized by a higher expression of metalloproteinases (MMTs), which break down the surrounding extracellular matrix and thus produce tunnels to the cell migration.

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