Many retinal degenerative diseases result in vision impairment or permanent blindness due to photoreceptor loss or dysfunction. It has been observed that Pde6b^rd1 mice (rd1), which carry a spontaneous nonsense mutation in the pde6b gene, have a strong phenotypic similarity to patients suffering from autosomal recessive retinitis pigmentosa. In this study, we present a novel mouse model of retinitis pigmentosa generated through pde6b gene knockout using CRISPR/Cas9 technology. We compare this Pde6b-KO mouse model to the rd1 mouse model to gain insights into the progression of retinal degeneration. The functional assessment of the mouse retina and the tracking of degeneration dynamics were performed using electrophysiological methods, while retinal morphology was analyzed through histology techniques. Interestingly, the Pde6b-KO mouse model demonstrated a higher amplitude of photoresponse than the rd1 model of the same age. At postnatal day 12, the thickness of the photoreceptor layer in both mouse models did not significantly differ from that of control animals; however, by day 15, a substantial reduction was observed. Notably, the decline in the number of photoreceptors in the rd1 model occurred at a significantly faster rate. These findings suggest that the C3H background may play a significant role in the early stages of retinal degeneration.

With the wide use of magnetic resonance imaging (MRI) in clinical practice, more attention is paid to corpus callosum hypoplasia in children with various central nervous system diseases, including the cerebral palsy. We compared the areas of corpus callosum segments on the mid-sagittal MR images of the children with cerebral palsy and a control group; full-term infants and preterm infants. During the postnatal development, overall callosum area naturally increases, but single segments change differently in both absolute and relative values. In the control group, the relative area of the splenium grew insignificantly, whereas for the genu, it was stable. Children with cerebral palsy also show age-specific growth, but the area of corpus callosum is smaller compared with equal age children in the control group. We found an increased relative area of corpus callosum genu and a decrease of anterior body and splenium in the cerebral palsy group compared with the control group. The kCC index shows higher values in the control group than in any age subgroup of children with cerebral palsy. Mean values for the control group steadily increase with age, whereas in the cerebral palsy group, they remain the same. For every age-specific group, the difference of kCC was statistically significant. Mean kCC index values depend on gestational age and are statistically lower in preterm infants compared with full-term infants. Selective corpus callosum hypoplasia found in the current research could be due to Wallerian degeneration or a decreased number of axons in some of its segments. This could be explained by the disruption of neurogenesis in certain cortical areas. The morphometric index kCC can be used to detect deviations in the corpus callosum structure associated with prematurity and cerebral palsy.