Triamcinolone does not alter glial cell activation in the experimentally detached rabbit retina.
OBJECTIVE
Retinal detachment induces neural and photoreceptor cell degeneration and fast activation of micro- (immune) and macroglial cells. Hypoxia caused by increased distance between the choriocapillaris and the neural retina, and retinal oedema during detachment, are factors causing gliotic responses and cell degeneration. Triamcinolone may inhibit some cellular responses that accompany hypoxia. Therefore, we investigated whether triamcinolone acetonide may be effective to reduce the gliotic alterations in the detached retina.


METHODS
Local retinal detachment in rabbit eyes was created by subretinal injection of sodium hyaluronate, and triamcinolone acetonide (8 mg) was applied intravitreally. Wholecell patch-clamp records from Muller cells and Ca2+ imaging from retinal wholemounts were carried out. Microglial/immune cells in the nerve-fiber layer of retinal wholemounts were labeled with Griffonia simplicifolia agglutinin (GSA) isolectin. Additionally, two morphological parameters which characterize microglial activation/immune cell infiltration were estimated: the cross-sectional area of the somata of the cells in the nerve-fiber layer and the number of cell processes which evolve from the soma.


RESULTS
Three days after detachment, gliotic alterations were apparent in Muller cells isolated from both detached and nondetached retinal areas, as indicated by the cellular hypertrophy, by the downregulation of the plasma membrane K+ conductance, and by the upregulation of intracellular Ca2+ responsiveness to stimulation of purinergic P2Y receptors. Intravitreal triamcinolone did not alter these gliotic alterations of Muller cells. Furthermore, triamcinolone could not inhibit the immune cell activation present in detached and attached retinal areas. However, intravitreal triamcinolone led to a strong decrease in the process number of GSA lectin-positive cells from detached retinas.


CONCLUSIONS
The results suggest that triamcinolone is ineffective to inhibit gliotic responses in the detached retina. However, the immune cell activation after detachment was partially influenced by triamcinolone.
Uckermann
Ortrud
O
Paul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany.
Pannicke
Thomas
T
Wiedemann
Peter
P
Reichenbach
Andreas
A
Bringmann
Andreas
A
Uhlmann
Susann
S
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009457:Neuroglia / Q000187:drug effects* / Q000473:pathology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D018048:Receptors, Purinergic P2 / Q000378:metabolism; D012160:Retina / Q000187:drug effects* / Q000503:physiopathology; D012163:Retinal Detachment / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D014221:Triamcinolone / Q000008:administration & dosage / Q000627:therapeutic use*
D005938:Glucocorticoids; D018048:Receptors, Purinergic P2; D014221:Triamcinolone; D011188:Potassium; D002118:Calcium