Figure 4
Hypothesized molecular pathways for glutamate release from astrocytes in sclerotic hippocampi. This diagram is constructed on the basis of molecules produced by genes whose expression was found to increase (outlined in red) in this study and those reported in other studies (outlined in blue; also see text) of human TLE. The figure also shows that many of the pathways could be activated through known initial precipitating factors of TLE. Abbreviations: CCL2, CCL3, and CCL4, CC family chemokines; CD44, CD44 antigen (homing function and Indian blood group system); CX3CL1, fractalkine; CXCR4, α-chemokine receptor; COX-2, cyclooxygenase-2; EP1,3, calcium mobilizing receptors for PGE2; ERK1,2, extracellular signal-related kinases; HA, hyaluronan; IL-1β, interleukin-1β; HSV, herpes simplex virus; HHV6, human herpes virus 6; IL-1R, interleukin 1 receptor; PGE2, prostaglandin E2; SDF1, stromal derived factor 1, also known as CXCL12; TLR, Toll-like receptor; TNFR, tumor necrosis factor receptor; TNF-α, tumor necrosis factor α.