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NEW STRATEGIES IN STROKE (STROKE (CORE (CBF less than 10-20% (necrotic…

- - - - necrotic cell death
- - - - GluR activation
        
        excessive glutamate release
        
        Ca2+ influx
        
        cascades of cell death
        
        activation of calpains and caspases
        
        oxidative stress
        
        activation of pro-apoptotic proteins: BaxPar-4p53
        
        membrane-permeability changes
        
        Ca2+ binding proteins
        
        parvalbumin
        calbindin
    - - osmotic swelling
        
        dendritic varicosities
        
        somatic swelling
        
        necrotic cell death
        
        Cl-
        
        EDEMA
      - redusing of Na+ influx
        
        voltage-sensitive sodium channels
        (VSSC) blockers;
        TTX
    - - damage even in abundant glucose supply
      - K+ channels types
        
        ATP-dependent K+ channels
        
        react on the depletion of ATP
      - increasing of exrtacellular K+
        
        5-hydroxydecanoate (5HD) -
        an inhibitor of mitochondrial K+ channels
    - - passive influx
      - through GABA-gated channels
      - hypofunction of outward transporters
      - hyperfunction of inward transporters
      - fail of Cl-ATPase to transport Cl- into the extracellular space
        
        switch of equilibrium reversal potential for Cl-