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Effect of manganese chloride on the neurochemical profile of the rat hypothalamus

Manganese (Mn2+)-enhanced magnetic resonance imaging studies of the neuronal pathways of the hypothalamus showed that information about the regulation of food intake and energy balance circulate through specific hypothalamic nuclei. The dehydration-induced anorexia (DIA) model demonstrated to be app...

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Bibliographic Details
Published in:Journal of cerebral blood flow and metabolism 2011-12, Vol.31 (12), p.2324-2333
Main Authors: Just, Nathalie, Cudalbu, Cristina, Lei, Hongxia, Gruetter, Rolf
Format: Article
Language:English
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Summary:Manganese (Mn2+)-enhanced magnetic resonance imaging studies of the neuronal pathways of the hypothalamus showed that information about the regulation of food intake and energy balance circulate through specific hypothalamic nuclei. The dehydration-induced anorexia (DIA) model demonstrated to be appropriate for studying the hypothalamus with Mn2+-enhanced magnetic resonance imaging. Manganese is involved in the normal functioning of a variety of physiological processes and is associated with enzymes contributing to neurotransmitter synthesis and metabolism. It also induces psychiatric and motor disturbances. The molecular mechanisms by which Mn2+ produces alterations of the hypothalamic physiological processes are not well understood. 1H-magnetic resonance spectroscopy measurements of the rodent hypothalamus are challenging due to the distant location of the hypothalamus resulting in limited measurement sensitivity. The present study proposed to investigate the effects of Mn2+ on the neurochemical profile of the hypothalamus in normal, DIA, and overnight fasted female rats at 14.1 T. Results provide evidence that γ-aminobutyric acid has an essential role in the maintenance of energy homeostasis in the hypothalamus but is not condition specific. On the contrary, glutamine, glutamate, and taurine appear to respond more accurately to Mn2+ exposure. An increase in glutamine levels could also be a characteristic response of the hypothalamus to DIA.
ISSN:0271-678X
1559-7016
DOI:10.1038/jcbfm.2011.92