دورية أكاديمية

Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice.

التفاصيل البيبلوغرافية
العنوان: Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice.
المؤلفون: Olopade FE; Department of Anatomy, College of Medicine, University of Ibadan, Ibadan, Nigeria., Femi-Akinlosotu OM; Department of Anatomy, College of Medicine, University of Ibadan, Ibadan, Nigeria., Dauda O; Department of Anatomy, College of Medicine, University of Ibadan, Ibadan, Nigeria., Obiako J; Department of Anatomy, College of Medicine, University of Ibadan, Ibadan, Nigeria., Olopade JO; Neuroscience Unit, Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria., Shokunbi MT; Department of Anatomy, College of Medicine, University of Ibadan, Ibadan, Nigeria.; Division of Neurological Surgery, Department of Surgery, University of Ibadan, Ibadan, Nigeria.
المصدر: The Journal of comparative neurology [J Comp Neurol] 2024 Feb; Vol. 532 (2), pp. e25578. Date of Electronic Publication: 2024 Jan 04.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wiley-Liss Country of Publication: United States NLM ID: 0406041 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1096-9861 (Electronic) Linking ISSN: 00219967 NLM ISO Abbreviation: J Comp Neurol Subsets: MEDLINE
أسماء مطبوعة: Publication: <2003-> : Hoboken, N.J. : Wiley-Liss
Original Publication: Philadelphia Wistar Institute of Anatomy and Biology
مواضيع طبية MeSH: Vanadium*/adverse effects , Hydrocephalus*/chemically induced , Hydrocephalus*/drug therapy, Animals ; Mice ; Gliosis/drug therapy ; Kaolin/adverse effects ; Neurons
مستخلص: Vanadium is a prevalent neurotoxic transition metal with therapeutic potentials in some neurological conditions. Hydrocephalus poses a major clinical burden in neurological practice in Africa. Its primary treatment (shunting) has complications, including infection and blockage; alternative drug-based therapies are therefore necessary. This study investigates the function and cytoarchitecture of motor and cerebellar cortices in juvenile hydrocephalic mice following treatment with varying doses of vanadium. Fifty juvenile mice were allocated into five groups (n = 10 each): controls, hydrocephalus-only, low- (0.15 mg/kg), moderate- (0.3 mg/kg), and high- (3.0 mg/kg) dose vanadium groups. Hydrocephalus was induced by the intracisternal injection of kaolin and sodium metavanadate administered by intraperitoneal injection 72hourly for 28 days. Neurobehavioral tests: open field, hanging wire, and pole tests, were carried out to assess locomotion, muscular strength, and motor coordination, respectively. The cerebral motor and the cerebellar cortices were processed for cresyl violet staining and immunohistochemistry for neurons (NeuN) and astrocytes (glial fibrillary acidic protein). Hydrocephalic mice exhibited body weight loss and behavioral deficits. Horizontal and vertical movements and latency to fall from hanging wire were significantly reduced, while latency to turn and descend the pole were prolonged in hydrocephalic mice, suggesting impaired motor ability; this was improved in vanadium-treated mice. Increased neuronal count, pyknotic cells, neurodegeneration and reactive astrogliosis were observed in the hydrocephalic mice. These were mostly mitigated in the vanadium-treated mice, except in the high-dose group where astrogliosis persisted. These results demonstrate a neuroprotective potential of vanadium administration in hydrocephalus. The molecular basis of these effects needs further exploration.
(© 2024 Wiley Periodicals LLC.)
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فهرسة مساهمة: Keywords: cerebellar cortex; hydrocephalus; motor cortex; neuroprotective; vanadium
المشرفين على المادة: 00J9J9XKDE (Vanadium)
24H4NWX5CO (Kaolin)
تواريخ الأحداث: Date Created: 20240104 Date Completed: 20240222 Latest Revision: 20240426
رمز التحديث: 20240426
DOI: 10.1002/cne.25578
PMID: 38175813
قاعدة البيانات: MEDLINE
الوصف
تدمد:1096-9861
DOI:10.1002/cne.25578