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Intestinal motility disorders are a common complication after surgery for neonatal intestinal atresia. Although intestinal atresia causes alterations in the enteric nervous system, especially in its inner structures (nervous fibers in the mucosa, submucous and deep muscular plexuses), how these alterations develop is unclear. The chick model is a useful research tool for investigating the ontogenesis of the enteric nervous system and the pathogenesis of congenital bowel diseases. More information is needed on the overlap between the developing enteric nervous system and intestinal atresia. Because vasoactive intestinal polypeptide and substance P are typical intestinal neuropeptides, and vasoactive intestinal polypeptide acts as a modulator in neurodevelopment and an inhibitor of smooth muscle cell proliferation, our aim in this study was to investigate the distribution of their immunoreactivity in the developing enteric nervous system of normal and experimental chick models. We studied gut specimens excised from normal chick embryos (aged 12-20 days) and experimental chick embryos (aged 15-20 days) that underwent surgical intervention on day 12 to induce intestinal atresia (atresic embryos) or simply to grasp the bowel loop (sham-operated embryos). In normal chick embryos we showed vasoactive intestinal polypeptide and substance P immunoreactivity from day 12 in the submucous and myenteric plexuses. The distribution of peptide immunoreactivity differed markedly in atresic and normal or sham-operated gut embryos. These differences especially affected the inner structures of the enteric nervous system of specimens proximal to atresia and were related to the severity of dilation. Because nerve structures in the gut wall mucosa and submucous and deep muscular plexuses play a role in motility control and stretch sensation in the intestinal wall, our findings in the chick embryo may help to explain how gut motility disorders develop after surgery for neonatal intestinal atresia. [ABSTRACT FROM AUTHOR]

Abstract: Alpha-synuclein is a 140 amino acids’ protein, widely expressed in the nervous system of different vertebrates and closely related with several neurodegenerative disorders. Although its pathological involvement is reported from long time, its physiological function and its role in neurodegeneration is not yet clear. Disposing of two new monoclonal antibodies, able to detect alpha-synuclein in different compartments of the neurons, the aim of this study is to create an anatomical map of the protein''s distribution in the central nervous system of C57 BL\6J mouse, the mouse strain most sensitive to 1-methyl 4-phenyl 1,2,3,6-tetrahydro pyridine neurotoxicity and widely used to apply toxic models of Parkinson disease. The two monoclonal antibodies confirm their ability in visualizing the protein in distinct compartments of the neurons, since 2E3 detects alpha-synuclein in the nerve cells’ fibers, whereas 3D5 preferentially in the neuronal nuclei. Both antibodies, instead, are able to show alpha-synuclein at the synaptic terminals. The protein is ubiquitary distributed in the brain, as well as in the spinal cord, but its sub-cellular localization differs markedly in the various regions of the central nervous system. Among alpha-synuclein immunoreactive territories, we describe a particular organization in habenular nuclei, dorsal hippocampus, olfactory bulbs, brain stem nuclei and cerebellar cortex. This preliminary immunohistochemical study, provides the first anatomical map of the alpha-synuclein distribution in the C57 BL\6J mouse CNS and suggests that alpha-synuclein is differentially localized, at sub-cellular level, in different types of neurons and that, therefore, it can plays a specific role for each neuronal subtype. Our study in healthy C57 BL/6J mice represents a starting point to analyze the variations in the overall distribution of alpha-synuclein in mouse models of Parkinson disease. [Copyright &y& Elsevier]