Wissenschaftliches Programm:
Freitag/Friday, 21. September 2007

Dozenten
Gerhardt H. (London)
Reichenbach A. (Leipzig)
Remé C. E. (Zürich)
Rungger-Brändle E. (Genf)
Thanos S. (Münster)
Yandiev Y. (Leipzig)

Each pathological event in the retina is associated with an activation of glial cells (astrocytes, Müller cells, and microglia). Müller cells constitute a functional link between neurons and blood vessels, involved in the regulation of the homeostasis of retinal ions and water (A. Reichenbach). Recent data suggest that dysfunction of Müller cells (P. Wiedemann) and activation of microglial cells (S. Thanos) may more directly contribute to retinal degeneration and edema development under pathological conditions. Via the release of vasoactive factors, Müller cells may control pathological angiogenesis (W. Eichler). Astrocytes guide the vessel growth during normal ontogenic retinal angiogenesis (H. Gerhardt). Alterations in the retinal vasculature in diabetes (H. Hammes), or light-induced photoreceptor apoptosis (Ch. Remé), cause similar gliotic responses in Müller cells (E. Rungger-Brändle; A. Bringmann), likely contributing to secondary retinal injury. The symposium is aimed at bridging normal development and pathological alterations of the retinal vasculature and glial cells, by presenting data which suggest that the inhibition of glial cell activation may represent a potential target for neuroprotective therapies.