Synapse and Receptor Alterations in Two Different S100B-Induced Glaucoma-Like Models.

Area of Science:

• Neuroscience
• Immunology
• Ophthalmology

Background:

• Glaucoma is characterized by irreversible retinal ganglion cell (RGC) loss and optic nerve damage.
• The immune system's role in glaucoma pathogenesis is increasingly recognized.
• S100B protein has been implicated in RGC death in experimental glaucoma models.

Purpose of the Study:

• To investigate synaptic alterations in two distinct S100B-induced glaucoma models.
• To compare the effects of intraocular S100B injection versus systemic S100B immunization on synapses.
• To explore the expression of NMDA and GABA receptors in these models.

Main Methods:

• Two rat models of glaucoma were established: intraocular S100B injection and systemic S100B immunization.
• Synaptic alterations were assessed 14 days post-induction.
• Immunohistochemistry was used to evaluate pre- and post-synaptic structures and receptor expression.

Main Results:

• Intraocular S100B injection led to degeneration of excitatory post-synapses.
• Excitatory pre-synapses decreased significantly with intraocular S100B and tended to increase with systemic immunization.
• Both NMDA and GABA receptors were significantly upregulated in S100B-treated animals in both models.

Conclusions:

• S100B protein significantly impacts synaptic integrity in experimental glaucoma.
• Upregulation of NMDA and GABA receptors may contribute to synapse degeneration.
• These findings highlight potential therapeutic targets for preserving vision in glaucoma.