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Graefes Arch Clin Exp Ophthalmol. 2016 Mar;254(3):497-503. doi: 10.1007/s00417-015-3250-5. Epub 2016 Jan 7.

Ischemic regulation of brain-derived neurotrophic factor-mediated cell volume and TrkB expression in glial (Müller) and bipolar cells of the rat retina.

Author information

1
Paul Flechsig Institute of Brain Research, Medical Faculty, University of Leipzig, Leipzig, Germany.
2
Department of Ophthalmology and Eye Hospital, Medical Faculty, University of Leipzig, Liebigstrasse 10-14, D-04103, Leipzig, Germany.
3
Institute of Anatomy, Histology and Embryology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany.
4
Department of Ophthalmology and Eye Hospital, Medical Faculty, University of Leipzig, Liebigstrasse 10-14, D-04103, Leipzig, Germany. bria@medizin.uni-leipzig.de.

Abstract

BACKGROUND:

Osmotic swelling of neurons and glial cells contributes to retinal edema and neurodegeneration. BDNF, a major neuroprotectant in the retina, was shown to inhibit osmotic swelling of glial (Müller) and bipolar cells in the rat retina; the effect of BDNF on the bipolar cell swelling is mediated by inducing a release of neuroprotective cytokines from Müller cells (Berk et al., Neuroscience 295:175-186, 2015). We determined whether BDNF-mediated cell volume regulation was altered after transient retinal ischemia.

METHODS:

Retinal slices from the eyes of rats that underwent a 1-h pressure-induced retinal ischemia and from control eyes were superfused with a hypoosmotic solution.

RESULTS:

Exogenous BDNF prevented osmotic swelling of Müller cells in both control and post-ischemic retinal slices. BDNF also prevented osmotic swelling of bipolar cells in the control retina, but not in the ischemic retina. On the other hand, exogenous bFGF prevented the swelling of both Müller and bipolar cells in the ischemic retina. Freshly isolated Müller cells of control retinas displayed immunoreactivity of truncated but not full-length TrkB. In contrast, Müller cells of post-ischemic retinas displayed immunoreactivity of both TrkB isoforms. Bipolar cells isolated from control and post-ischemic retinas were immunolabeled for both TrkB isoforms.

CONCLUSIONS:

The data may suggest that the ischemic abrogation of the BDNF effect in bipolar cells is related to altered BDNF receptor expression in Müller cells. Glial upregulation of full-length TrkB may support the survival of Müller cells in the ischemic retina, but may impair the BDNF-induced release of neuroprotective cytokines such as bFGF from Müller cells.

KEYWORDS:

BDNF; Bipolar cell; Glia; Ischemia; Retina; TrkB

PMID:
26743749
DOI:
10.1007/s00417-015-3250-5
[Indexed for MEDLINE]

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