Summary. In Xenopus laevis Daudin the anlage of the carotid labyrinth, a baro- and chemoreceptor, appears in early premetamorphosis (NF stage 53) as a swelling of the third aortic arch at the point where the common carotid artery gives off the external carotid artery. A conspicuous accumulation of melanocytes preceeds the formation of the labyrinth maze which starts to grow at the end of metamorphic climax (NF stage 64) and continues so through juvenile age. In adult animals the carotid labyrinth displays a spherical to ovoid shape, has an average length of 1.4 mm, a width of about 0.8 mm and a height of about 0.4 mm. The maze vessels form by sprouting angiogenesis from the common carotid artery and the internal carotid artery. Scanning electron microscopy of vascular corrosion casts reveals that size, overall shape, surface morphology and vascular patterns of the carotid labyrinth vary greatly between individuals, whereby intussusceptive microvascular growth (= nonsprouting angiogenesis) and its facets model and contribute to the maturation of the labyrinth’s final vascular patterns. Key words: Xenopus, carotid labyrinth, vascular anatomy, vascular casts, histomorphology
Summary. Neonatal hypoxic/ischemic (H/I) brain injury causes neurological impairment, including cognitive and motor dysfunction as well as seizures. Patterns of H/I injury-induced neuron death using rodent models are considered to be similar to the cases in human H/I encephalopathy. The participation of autophagy in neuron death has been a common feature in neonatal rodent models of H/I brain injury and human H/I encephalopathy when examined by immunochemical approaches for MAP1-LC3. This tendency has also been confirmed in neuronal tissue-specific Atg7 conditional knockout mice. However, while the current rat H/I model that is used for analyzing autophagy results in global damage to the ipsilateral hemisphere, it does not entirely reflect the neuropathological changes that appear in the neonatal mouse H/I model, in which the hippocampus is selectively damaged. The present study established a neonatal rat model of H/I injury with a milder ischemic insult, in which autophagy was involved in the hippocampal CA1region after H/I injury when examined by electron microscopy, and by immunohistochemical and biochemical analyses of LC3.
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