Alpha-tocopherol, an exogenous factor of adult hippocampal neurogenesis regulation.
In previous work, we found that adult hippocampal neurogenesis in rat is affected by vitamin E deficiency. Because vitamin E deficiency is a complex condition involving numerous biological systems, it is possible that its effect on postnatal new neuron production could be mediated by unknown changes in different factors that in turn play a role in this process. To clarify if vitamin E plays a direct role in regulating hippocampal neurogenesis, we studied the neurogenesis in adult control rats and in adult rats under supplementation with alpha-tocopherol, the most important compound of vitamin E. The alpha-tocopherol level in control and supplemented rats was monitored. Qualitative and quantitative analysis of cell proliferation and death was carried out and expression of immature neuron markers PSA-NCAM, TUC 4, and DCX was investigated in hippocampus dentate gyrus. alpha-Tocopherol levels increased significantly in both plasma and brain after supplementation. Cell proliferation was inhibited in alpha-tocopherol-supplemented rats, the number of dying cells was reduced, and the number of cells expressing the immature neuron markers was increased. The results obtained confirm and extend the idea that vitamin E is an exogenous factor playing a direct role in regulation of different steps of adult hippocampal neurogenesis. Some hypotheses about the possible mechanisms underlying the complex action of alpha-tocopherol, related to its antioxidant and molecule-specific non-antioxidant properties, are proposed and discussed.
Cecchini
Tiziana
T
Institute of Morphological Sciences, University of Urbino, Urbino, Italy. t.cecchini@uniurb.it
Ciaroni
Sandra
S
Ferri
Paola
P
Ambrogini
Patrizia
P
Cuppini
Riccardo
R
Santi
Spartaco
S
Del Grande
Paolo
P
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001923:Brain Chemistry; D001973:Bromodeoxyuridine / Q000378:metabolism / Q000493:pharmacokinetics; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism; D064026:Calbindins; D002452:Cell Count; D016923:Cell Death; D002455:Cell Division; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D000089622:Doublecortin Domain Proteins; D000089662:Doublecortin Protein; D029721:Drosophila Proteins; D005455:Fluorescent Antibody Technique; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D020287:In Situ Nick-End Labeling / Q000379:methods; D008025:Ligases / Q000378:metabolism; D008297:Male; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins / Q000378:metabolism; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism; D011838:Radiation-Sensitizing Agents / Q000378:metabolism / Q000493:pharmacokinetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D012794:Sialic Acids / Q000378:metabolism; D013997:Time Factors; D044767:Ubiquitin-Protein Ligases; D024502:alpha-Tocopherol / Q000097:blood / Q000494:pharmacology*
D000975:Antioxidants; D029742:Caenorhabditis elegans Proteins; D064026:Calbindins; C000714848:Dcx protein, rat; D000089622:Doublecortin Domain Proteins; D000089662:Doublecortin Protein; D029721:Drosophila Proteins; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D039842:Neural Cell Adhesion Molecule L1; D009479:Neuropeptides; D011838:Radiation-Sensitizing Agents; D064030:S100 Calcium Binding Protein G; D012794:Sialic Acids; C103469:polysialyl neural cell adhesion molecule; D044767:Ubiquitin-Protein Ligases; C071006:neur protein, Drosophila; D008025:Ligases; D001973:Bromodeoxyuridine; D024502:alpha-Tocopherol