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Magnesium deficiency induces anxiety and HPA axis dysregulation: modulation by therapeutic drug treatment.

Sartori SB, Whittle N, Hetzenauer A, Singewald N - Neuropharmacology (2011)

Bottom Line: Since there is evidence that Mg(2+) modulates the hypothalamic-pituitary adrenal (HPA) axis, we tested whether enhanced anxiety-like behaviour can be reliably elicited by dietary Mg(2+) deficiency and whether Mg(2+) deficiency is associated with altered HPA axis function.It is further suggested that dysregulations in the HPA axis may contribute to the hyper-emotionality in response to dietary induced hypomagnesaemia.This article is part of a Special Issue entitled 'Anxiety and Depression'.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, Institute of Pharmacy, and Centre for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Peter-Mayr-Strasse 1, A-6020 Innsbruck, Austria. simone.sartori@uibk.ac.at

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In the hyponeophagia test, the latency to eat a preferred food placed in the centre of the testing arena and the distance travelled is shown for C57Bl/6N mice fed either the control diet (control; n = 19), the Mg2+ deficient diet (MgD; n = 16), or the Mg2+ deficient diet and additional long-term treatment with either desipramine (MgD + DMI; n = 12) or paroxetine (MgD + PAR; n = 16). Data represent means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for drug-treated Mg2+ deficient mice vs. Mg2+ deficient mice.
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fig2: In the hyponeophagia test, the latency to eat a preferred food placed in the centre of the testing arena and the distance travelled is shown for C57Bl/6N mice fed either the control diet (control; n = 19), the Mg2+ deficient diet (MgD; n = 16), or the Mg2+ deficient diet and additional long-term treatment with either desipramine (MgD + DMI; n = 12) or paroxetine (MgD + PAR; n = 16). Data represent means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for drug-treated Mg2+ deficient mice vs. Mg2+ deficient mice.

Mentions: Next, we subjected all C57Bl/6N mice to the hyponeophagia paradigm, one of the few tests which are sensitive to the anxiolytic effects of chronic antidepressant treatment (Bodnoff et al., 1989; Dulawa and Hen, 2005; Gordon and Hen, 2004). There was a significant group effect in the latency to eat (F3,58 = 11.828, P < 0.001) the preferred food placed into the centre of the testing arena (Fig. 2). Mg2+ deficiency caused an increase in the latency to eat. In Mg2+ deficient mice chronic desipramine treatment reduced the latency to eat compared with untreated mice while long-term treatment with paroxetine did not affect this behavioural parameter (Fig. 2). Mg2+ deficiency and long-term antidepressant treatments did not alter general locomotor activity as indicated by the distances travelled in the open field test (n.s.; Table 1), the light/dark test (n.s.; Table 1), and the hyponeophagia test (n.s.; Fig. 2). All together these findings suggest that chronic Mg2+ deficiency was anxiogenic and that chronic desipramine, but not paroxetine treatment was effective in reducing anxiety in this model.


Magnesium deficiency induces anxiety and HPA axis dysregulation: modulation by therapeutic drug treatment.

Sartori SB, Whittle N, Hetzenauer A, Singewald N - Neuropharmacology (2011)

In the hyponeophagia test, the latency to eat a preferred food placed in the centre of the testing arena and the distance travelled is shown for C57Bl/6N mice fed either the control diet (control; n = 19), the Mg2+ deficient diet (MgD; n = 16), or the Mg2+ deficient diet and additional long-term treatment with either desipramine (MgD + DMI; n = 12) or paroxetine (MgD + PAR; n = 16). Data represent means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for drug-treated Mg2+ deficient mice vs. Mg2+ deficient mice.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3198864&req=5

fig2: In the hyponeophagia test, the latency to eat a preferred food placed in the centre of the testing arena and the distance travelled is shown for C57Bl/6N mice fed either the control diet (control; n = 19), the Mg2+ deficient diet (MgD; n = 16), or the Mg2+ deficient diet and additional long-term treatment with either desipramine (MgD + DMI; n = 12) or paroxetine (MgD + PAR; n = 16). Data represent means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for drug-treated Mg2+ deficient mice vs. Mg2+ deficient mice.
Mentions: Next, we subjected all C57Bl/6N mice to the hyponeophagia paradigm, one of the few tests which are sensitive to the anxiolytic effects of chronic antidepressant treatment (Bodnoff et al., 1989; Dulawa and Hen, 2005; Gordon and Hen, 2004). There was a significant group effect in the latency to eat (F3,58 = 11.828, P < 0.001) the preferred food placed into the centre of the testing arena (Fig. 2). Mg2+ deficiency caused an increase in the latency to eat. In Mg2+ deficient mice chronic desipramine treatment reduced the latency to eat compared with untreated mice while long-term treatment with paroxetine did not affect this behavioural parameter (Fig. 2). Mg2+ deficiency and long-term antidepressant treatments did not alter general locomotor activity as indicated by the distances travelled in the open field test (n.s.; Table 1), the light/dark test (n.s.; Table 1), and the hyponeophagia test (n.s.; Fig. 2). All together these findings suggest that chronic Mg2+ deficiency was anxiogenic and that chronic desipramine, but not paroxetine treatment was effective in reducing anxiety in this model.

Bottom Line: Since there is evidence that Mg(2+) modulates the hypothalamic-pituitary adrenal (HPA) axis, we tested whether enhanced anxiety-like behaviour can be reliably elicited by dietary Mg(2+) deficiency and whether Mg(2+) deficiency is associated with altered HPA axis function.It is further suggested that dysregulations in the HPA axis may contribute to the hyper-emotionality in response to dietary induced hypomagnesaemia.This article is part of a Special Issue entitled 'Anxiety and Depression'.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, Institute of Pharmacy, and Centre for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Peter-Mayr-Strasse 1, A-6020 Innsbruck, Austria. simone.sartori@uibk.ac.at

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Related in: MedlinePlus