{'fraction_non_alphanumeric': 0.034552845528455285, 'fraction_numerical': 0.009485094850948509, 'mean_word_length': 5.421739130434783, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Synaptic pathology of outer retina in Ccl2/Cx3cr1 deficient mice

Age‐related macular degeneration (AMD) is the leading cause of blindness among the elderly. Although various AMD mice models exhibit retinal pathology, there are limited reports about synaptic morphology in these models. We investigate the synaptic pathology of outer retina in C57BL/6 (wild type) and Ccl2−/−/Cx3cr1−/− (DKO) mice, a model with AMD‐like retinal lesions, at various ages by light and electron microscopy (EM). The labeling of CtBP2, a presynaptic ribbon protein, was discontinuous and interrupted by areas with few punctas. Some CtBP2 punctas were visible in the outer nuclear layer (ONL) at one month old. Consistently, a few calbindin‐labeled horizontal processes and occasionally PKC‐labeled rod bipolar dendrites extended aberrantly into the ONL. These aberrant ribbons and processes increased in numbers with ages. Double labeling studies showed close associations of synaptic ribbons with either horizontal or rod bipolar processes. EM showed a significant decrease of cone synapses in DKO mice compared to the WT mice. Furthermore, it confirmed that aberrant horizontal and bipolar processes made synaptic contacts with photoreceptor terminals. We conclude that, in addition to presynaptic photoreceptor terminals degeneration, horizontal and bipolar processes sprout to form ectopic synapses in the ONL of Ccl2−/−/Cx3cr1−/− mice, suggesting a neuronal remodeling in the retinal lesions.