Cellular Neurophysiology

Schematic representation of the proposed mechanism during GO(a) and rGO(b) stimulation and the resulting astrocyte response. a) In GO, charge buildup at the GO–cell interface depolarizes the membrane (1), activating VGCCs and TRPA1 and enabling external Ca2+ influx (2). This triggers internal Ca2+ release via IP3 and SERCA, but not RyR (3). IP3 further enhances TRPV4-mediated Ca2+ influx (4), leading to sustained cytoplasmic Ca2+ elevation with an S-type signal. TRPA1 may help maintain or amplify Ca2+ influx. b) In rGO, charge accumulates at the cell-solution interface, causing membrane depolarization at the electrolyte-cell boundary (1), potentially triggering ER-mediated internal Ca2+ release (2). The electric field may also repel cations, reducing external Ca2+ influx (3).

Scheme describing possible directions of NG2 glial differentiation after ischemic brain injury. Five subpopulations of NG2 glia were identified in mouse brain cortex in healthy tissue (green) and after focal cerebral ischemia (FCI; red). Four of these populations correspond to oligodendrocyte precursors at different stages of differentiation. The fifth population expresses markers of astrocytes as well as neuronal precursors. The number of cells of the fifth population increases after FCI. NeuN-positive cells (matured neurons) which probably developed from the original population of NG2 glia, are present in the brain 28 days after FCI.

Scheme describing the major changes in astrocyte channel/transporter expression and extracellular matrix structure resulting in the altered ability of astrocytes to uptake ions and neurotransmitters from the extracellular space (ECS) and regulate their cell volume. Schematic illustration of astrocyte morphological changes, extracellular matrix structure, and changes in astrocytic channel and transporter expression in Ctrl (A) and triple transgenic (3xTgAD) mouse models of Alzheimer's disease (B).

Graphical representation of the changes observed in adult mice. According to our immunohistochemical analyses, Wnt signaling inhibition (dnTCF4 or Dkk1) led to the differentiation of neural stem/progenitor cells to astrocytes, while activation of the pathway (constitutively active β-catenin) promoted neurogenesis. A similar impact of Wnt signaling modulation after ischemia was also confirmed by the patch-clamp technique. Larger cells represent a greater effect of Wnt signaling after ischemia. Abbreviations: Dkk1 – Dickkopf 1; dnTCF4 – dominant negative T-cell factor 4.