AUTHOR=Femi-Akinlosotu Omowumi Moromoke , Olopade Funmilayo Eniola , Obiako Jane , Olopade James Olukayode , Shokunbi Matthew Temitayo 

TITLE=Vanadium improves memory and spatial learning and protects the pyramidal cells of the hippocampus in juvenile hydrocephalic mice

JOURNAL=Frontiers in Neurology

VOLUME=Volume 14 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2023.1116727

DOI=10.3389/fneur.2023.1116727

ISSN=1664-2295

ABSTRACT=Background: Hydrocephalus is a neurological condition known to cause learning and memory disabilities due to its damaging effect on the hippocampal pyramidal neurons. Vanadium at low doses improves learning and memory abilities in neurological disorders but uncertain whether such protection will be provided in hydrocephalus. We investigated the morphology of these neurons and neurobehaviour in vanadium-treated and control juvenile hydrocephalic mice.
Methods: Hydrocephalus was induced by intra-cisternal injection of sterile-kaolin into juvenile mice which were allocated into 4 groups of 10 pups each, one group served as an untreated hydrocephalic control while others were treated with 0.15, 0.3 and 3mg/kg i.p of vanadium compound respectively, starting 7days post-induction for 28days. Non-hydrocephalic sham controls (n=10) were sham operated without any treatment. Y-maze, Morris Water Maze and Novel Object Recognition tests were carried out before the sacrifice, the brains harvested, and processed for Cresyl Violet and immunohistochemistry for neurons (NeuN) and astrocytes (GFAP). The pyramidal neurons of the CA1 and CA3 regions of the hippocampus were assessed qualitatively and quantitatively. Data were analyzed using GraphPad prism 8.
Results: Escape latencies of vanadium-treated groups were significantly shorter (45.30±26.30s; 46.50±26.35s; 42.99±18.44s) than untreated group (62.06±24.02s) suggesting improvements in learning abilities. Time spent in the correct quadrant was significantly shorter in the untreated group (21.19±4.15s) compared to control (34.15±9.44s) and 3mg/kg vanadium-treated group (34.35±9.74s). Recognition index and mean % alternation were lowest in untreated group (p=0.0431; p=0.0158) suggesting memory impairments, with insignificant improvements in vanadium-treated groups. NeuN immuno-stained CA1 revealed loss of apical processes of the pyramidal cells in untreated hydrocephalus group relative to control and a gradual reversal attempt in the vanadium-treated groups. Astrocytic activation in the untreated hydrocephalus group were attenuated in the vanadium-treated groups under the GFAP stain. Pyknotic index in CA1 pyramidal layer of untreated (18.82±2.59) and 0.15mg/kg vanadium-treated groups (18.14±5.92) were significantly higher than control (11.11±0.93; p=0.0205; p=0.0373) while there was no significant difference in CA3 pyknotic index across all groups.
Conclusion: Our results suggest that vanadium has a dose-dependent protective effect on the pyramidal cells of the hippocampus and on memory and spatial learning functions in juvenile hydrocephalic mice