THE MODULATION OF RETINAL SEROTONIN SIGNALLING PATHWAYS USING SELECTIVE SEROTONIN REUPTAKE INHIBITORS AFFECTS THE EXPRESSION OF BDNF AND CONDUCTIVITY OF ELECTRIC SYNAPSES AND PREVENTS RETINAL GANGLION CELL DEATH
Selective serotonin reuptake inhibitors have shown many antiapoptotic and neuroprotective effects by increasing BDNF content in the retina and by reducing conductivity of electrical synapses, thus limiting secondary neurodegeneration of Retinal Ganglion Cells (RGC) and retinal interneurons (RI). Fou...
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Published in | Acta neurobiologiae experimentalis Vol. 82; p. XLII |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
Warsaw
Polish Academy of Sciences
01.01.2022
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Subjects | |
Online Access | Get full text |
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Summary: | Selective serotonin reuptake inhibitors have shown many antiapoptotic and neuroprotective effects by increasing BDNF content in the retina and by reducing conductivity of electrical synapses, thus limiting secondary neurodegeneration of Retinal Ganglion Cells (RGC) and retinal interneurons (RI). Fourteen Long-Evans rats were treated orally with Escitalopram or PBS for 12 weeks. After 8 weeks, transient elevation of intraocular pressure was inducted in the right eye in order to induce retinal ischemia (IC). Electroretinography (ERG) was performed in a few time points. Four weeks later, rats were sacrificed and retinas and optic nerves were isolated. A loss of RGC density was noted in the ischemic retina treated with PBS that was not noticed in the group treated with Escitalopram (261±118 vs. 392±92 p<0,05). In the Escitalopram-treated group, scotopic amplitudes of all oscillatory potentials (OP) measured in ERG were significantly higher 14 days after IC induction (p<0,05), while in the control group deep disturbance of RI function was observed, expressed in significant reduction of OP amplitudes (p<0.05). Oral treatment with Escitalopram prevents desynchronization of RI function during ischemic conditions in a rat model. Observations presented above may become crucial for new therapeutic methods for vascular pathologies of the retina. |
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ISSN: | 0065-1400 1689-0035 |