Retinal neurons, as part of the central nervous system, are unable to regenerate in response to damage. Glaucoma, a progressive optic neuropathy, is the leading cause of severe visual impairment or permanent vision loss. The World Health Organization has recognized glaucoma as a social disease, which is the leading cause of irreversible blindness in the world. The exact mechanism of Retinal Ganglion Cells death in glaucoma is still unknown, although apoptosis has been suggested as the major mechanism.

Connexins are important channel proteins that form gap junctions (electrical synapses). They coordinate metabolic and electrical functions of cells, including proliferation, differentiation, survival, and apoptosis. Electrical synapses enable the transport of small molecules, ions, and secondary messengers between cells, synchronizing the propagation of an action potential in excitable cell systems. In our studies to date, we have demonstrated the presence of gap junctions between the proximal, unmyelinated sections of RGC axons.

Despite the undoubted importance of electrical synapses in neuronal homeostasis, the expression of connexins correlates with the progression of neurodegenerative diseases. The reason for this is that electrical synapses can promote the spread the apoptotic signals leading to secondary neurodegeneration.

The aim of this study is to assess the transport and degradation pathways of the neuronal connexins Cx36 and Cx45 under physiological conditions and NMDA-induced cell stress.