![]() Furthermore, melatonin rescued the reduction of melatonin receptor expression. ANA‐12, a TrkB receptor antagonist, antagonized these melatonin actions and reduced melatonin‐induced neuroprotection. Moreover, melatonin increased BDNF and downstream phospho‐TrkB/Akt/ERK/CREB levels. ![]() Additionally, elevated cleaved caspase‐3 and Bax protein levels and reduced Bcl‐2 protein levels in response to hypoxia‐ischemia were diminished after melatonin treatment. Meanwhile, melatonin recovered visual dysfunction, as reflected by the improved amplitudes and implicit times of a‐wave, b‐wave, and oscillatory potentials. Melatonin helped maintain relatively normal inner retinal architecture and thickness and preserve inner retinal neuron populations in avascular areas by rescuing retinal ganglion and bipolar cells, and horizontal and amacrine neurons, from apoptosis. During this study, we used the oxygen‐induced retinopathy mice model to mimic retinal hypoxia‐ischemia phenotypes to investigate further the neuroprotective effect of melatonin on neonatal retinal neurons. Retinopathy of prematurity is a vision‐threatening disease associated with retinal hypoxia‐ischemia, leading to the death of retinal neurons and chronic neuronal degeneration.
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