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Kaolin-induced hydrocephalus causes acetylcholinesterase activity dysfunction following hypothalamic damage in infant rats

•Progressive ventricular dilatation causes hypothalamic damage in infant rats.•Hypothalamus shows neurotransmission impairment and decreased anti-apoptotic markers.•Cholinergic dysfunction may suggest hormonal disturbances in hydrocephalus. In hydrocephalus, the progressive accumulation of cerebrosp...

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Published in:Brain research 2019-12, Vol.1724, p.146408-146408, Article 146408
Main Authors: Catalão, Carlos Henrique Rocha, Souza, Anderson Oliveira, Santos-Júnior, Nilton Nascimento, da Silva, Stephanya Covas, da Costa, Luís Henrique Angenendt, Alberici, Luciane Carla, Rocha, Maria José Alves, da Silva Lopes, Luiza
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Language:English
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Summary:•Progressive ventricular dilatation causes hypothalamic damage in infant rats.•Hypothalamus shows neurotransmission impairment and decreased anti-apoptotic markers.•Cholinergic dysfunction may suggest hormonal disturbances in hydrocephalus. In hydrocephalus, the progressive accumulation of cerebrospinal fluid (CSF) causes dilatation of the lateral ventricles affecting the third ventricle and diencephalic structures such as the hypothalamus. These structures play a key role in the regulation of several neurovegetative functions by the production of the hormones. Since endocrine disturbances are commonly observed in hydrocephalic children, we investigated the impact of progressive ventricular dilation on the hypothalamus of infant rats submitted to kaolin-induced hydrocephalus. Seven-day-old infant rats were submitted to hydrocephalus induction by kaolin 20% injection method. After 14 days, the animals were decapitated and brain was collected to analyze mitochondrial function, neuronal activity by acetylcholinesterase (AChE) enzyme, oxidative damage, glial activation, and, neurotransmission-related proteins and anti-apoptotic processes in the hypothalamus. The hydrocephalic animals showed reduction in respiratory rates in the States of phosphorylation (P 
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2019.146408