Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Brattleboro homozygous diabetes insipidus (HOM-DI) mutant rat, incapable of synthesizing the neuropeptide vasopressin, has an impaired body growth of which the severity depends upon the conditions of reproduction. The comparison of homogeneously genotyped litters of HOM-DI and heterozygous (HET-DI) control pups, delivered and nursed by HOM-DI females, was regarded to be the only experimental design that practically excludes other influences on growth differences than the mutation itself. In this breeding scheme the postnatal growth of the HOM-DI brain is impaired, and the weight deficit persists into adulthood. Regionally, the neonatal development of cerebellum and medulla oblongata is most affected, and only slightly that of the cerebral cortex. The other separately isolated parts of the the brain seem to be unaffected (olfactory bulbs, hypothalamus, hippocampus, colliculi and thalamus plus basal ganglia). Cerebellum appeared to be the most consistently affected brain area of the HOM-DI Brattleboro rat since, unlike in the case of cerebral cortex and medulla oblongata, the weight deficit persisted throughout life. Olfactory bulb growth, on the other hand, appeared to continue after the first month of life, resulting in an increased weight at day 180. Water content of cerebral cortex and cerebellum of HOM-DI adults appeared slightly higher and might be explained by the generation of different brain water regulation systems for HET- and HOM-DI Brattleboro rats. Protein and DNA estimations of cerebral cortex, cerebellum and olfactory bulbs of male brains during development and in adulthood reflect the differences as found for weight, indicating no obvious changes in cell densities. It is concluded after comparison with other types of brain growth malformations, that the HOM-DI Brattleboro brain has its own particular etiology. The possible involvement of the action of vasopressin is postulated and discussed.
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PMID:Impaired brain development of the diabetes insipidus Brattleboro rat. 707 63

This review considers a link between prematurity and autism by comparing symptoms, physiological abnormalities, and behavior. It focuses on the bidirectional signaling between the microbiota and the brain, here defined as the microbiota-gut-vagus-heart-brain (MGVHB) axis and its systemic disruption accompanying altered neurodevelopment. Data derived from clinical and animal studies document increased prevalence of gastrointestinal, cardiovascular, cognitive, and behavioral symptoms in both premature and autistic children and suggest an incomplete maturation of the gut-blood barrier resulting in a "leaky gut," dysbiosis, abnormalities in vagal regulation of the heart, altered development of specific brain regions, and behavior. Furthermore, this review posits the hypothesis that common genetic variants link the abnormalities in the MGVHB axis in premature and autistic pathologies. This hypothesis is based on the recently identified common genetic variants: early B cell factor 1 (EBF1), selenocysteine tRNA-specific eukaryotic elongation factor (EEFSEC), and angiotensin II receptor type 2 (AGTR2), in the maternal and infant DNA samples, associated with risk of preterm birth and independently implicated in a risk of autism. We predict that the AGTR2 variants involved in the brain maturation and oxytocin-arginine-vasopressin (OXT-AVP) pathways, related to social behavior, will contribute to our understanding of the link between prematurity and autism paving a way to new therapies.
Cerebellum 2019 Apr
PMID:Common Genetic Variants Link the Abnormalities in the Gut-Brain Axis in Prematurity and Autism. 3010 1