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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Rocha Catalao, Carlos Henrique [1] ; Souza, Anderson Oliveira [2] ; Santos-Junior, Nilton Nascimento [1] ; da Silva, Stephanya Covas [3] ; Angenendt da Costa, Luis Henrique [1] ; Alberici, Luciane Carla [2] ; Alves Rocha, Maria Jose [4] ; Lopes, Luiza da Silva [3]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Neurosci & Behav Sci, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Sch Pharmaceut Sci Ribeirao Preto, Dept Phys & Chem, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Surg & Anat, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Sch Dent Ribeirao Preto, Dept Morphol Physiol & Basic Pathol, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Brain Research; v. 1724, DEC 1 2019.
Web of Science Citations: 0
Abstract

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 < 0.01) and non-phosphorylation (P < 0.05); increase in AChE activity in both the cytosol (P < 0.05) and the membrane (P < 0.01); decrease in synaptophysin (P < 0.05) and Bcl-2 (P < 0.05) contents and; increase in protein carbonyl (P < 0.01), GFAP (P < 0.01) and lba-1 (P < 0.05) levels. The results demonstrate that ventricular dilation causes hypothalamic damage characterized by cholinergic dysfunction and suggests further investigation of the synthesis and secretion of hormones to generate new approaches and to assist in the treatment of hydrocephalic patients with hormonal alterations. (AU)

FAPESP's process: 16/23509-4 - Identification of neuroprotective myokines released by human skeletal muscle at low and high intensity contractions: role of mitochondrial bioenergetics and oxidative stress
Grantee:Luciane Carla Alberici
Support Opportunities: Regular Research Grants
FAPESP's process: 16/11212-7 - Role of hyperbaric oxygen therapy in the control of brain lesions in experimental hydrocephalus
Grantee:Luiza da Silva Lopes
Support Opportunities: Regular Research Grants