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Abstract #90509 Published in IGR 21-3
Synapse and Receptor Alterations in Two Different S100B-Induced Glaucoma-Like Models
Benning L; Reinehr S; Grotegut P; Kuehn S; Stute G; Dick HB; Joachim SCInternational journal of molecular sciences 2020; 21:
Glaucoma is identified by an irreversible retinal ganglion cell (RGC) loss and optic nerve damage. Over the past few years, the immune system gained importance in its genesis. In a glaucoma-like animal model with intraocular S100B injection, RGC death occurs at 14 days. In an experimental autoimmune glaucoma model with systemic S100B immunization, a loss of RGCs is accompanied by a decreased synaptic signal at 28 days. Here, we aimed to study synaptic alterations in these two models. In one group, rats received a systemic S100B immunization ( = 7/group), while in the other group, S100B was injected intraocularly ( = 6-7/group). Both groups were compared to appropriate controls and investigated after 14 days. While inhibitory post-synapses remained unchanged in both models, excitatory post-synapses degenerated in animals with intraocular S100B injection ( = 0.03). Excitatory pre-synapses tendentially increased in animals with systemic S100B immunization ( = 0.08) and significantly decreased in intraocular ones ( = 0.04). Significantly more -methyl-d-aspartate (NMDA) receptors (both ≤ 0.04) as well as gamma-aminobutyric acid (GABA) receptors (both < 0.03) were observed in S100B animals in both models. We assume that an upregulation of these receptors causes the interacting synapse types to degenerate. Heightened levels of excitatory pre-synapses could be explained by remodeling followed by degeneration.
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.
Full articleClassification:
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
11.8 Neuroprotection (Part of: 11 Medical treatment)