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. 2006 Nov 16;103(48):18326–18331. doi: 10.1073/pnas.0605077103

Fig. 3.

Fig. 3.

Neuronal injury, glial activation, and activation of Smad signaling after excitotoxic brain injury. SBE-luc mice (T9-7F) were lesioned with KA (20 mg/kg, s.c.) and killed 1, 3, and 5 days later. (A) Time course of KA-induced neuronal injury (cresyl violet staining), activation of Smad signaling (Smad2P immunostaining), astroglial activation (GFAP immunostaining), and microglial activation (CD68 immunostaining). (B) Confocal microscope images of double immunofluorescence with antibodies against Smad2P (24) (green) and cell type-specific markers NeuN, CD68, or GFAP (red). Smad2P-expressing cells appear yellow after superimposition.