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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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Effect of Mg2+ deficiency and diazepam treatment (1 mg/kg, i.p.) on behaviour and c-Fos expression in the paraventricular hypothalamic nucleus (PVN) of BALB/c mice following exposure to the open arm of an elevated plus maze. A. In mice fed a Mg2+ restricted diet the anxiety-related behaviour was elevated as indicated by the number of entries into the (anxiogenic) distal compartment of the open arm. Treatment with diazepam normalised this anxious phenotype. B. Compared with vehicle-treated controls, c-Fos induction was increased in the magnocellular portion of the PVN in Mg2+ deficient mice and was reversed by diazepam treatment. C. Representative photograph (scale bar = 100 μm) showing delineation of the PVN regions analysed with the help of a mouse brain atlas (Paxinos and Franklin, 2001). D. High magnification photograph showing c-Fos-positive cells in the magnocellular portion of the PVN in all experimental groups. Data represent mean ± SEM. n = 10 per experimental group. *P < 0.05, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for diazepam vs. vehicle. 3V: third ventricle; DZP: diazepam; magno: magnocellular portion of the PVN; parvo: parvocellular portion of the PVN; V: vehicle.
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fig4: Effect of Mg2+ deficiency and diazepam treatment (1 mg/kg, i.p.) on behaviour and c-Fos expression in the paraventricular hypothalamic nucleus (PVN) of BALB/c mice following exposure to the open arm of an elevated plus maze. A. In mice fed a Mg2+ restricted diet the anxiety-related behaviour was elevated as indicated by the number of entries into the (anxiogenic) distal compartment of the open arm. Treatment with diazepam normalised this anxious phenotype. B. Compared with vehicle-treated controls, c-Fos induction was increased in the magnocellular portion of the PVN in Mg2+ deficient mice and was reversed by diazepam treatment. C. Representative photograph (scale bar = 100 μm) showing delineation of the PVN regions analysed with the help of a mouse brain atlas (Paxinos and Franklin, 2001). D. High magnification photograph showing c-Fos-positive cells in the magnocellular portion of the PVN in all experimental groups. Data represent mean ± SEM. n = 10 per experimental group. *P < 0.05, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for diazepam vs. vehicle. 3V: third ventricle; DZP: diazepam; magno: magnocellular portion of the PVN; parvo: parvocellular portion of the PVN; V: vehicle.

Mentions: In an attempt to gain additional evidence for a possible functional relevance of increased PVN prepro-CRH mRNA expression in the Mg2+ deficiency-induced enhanced anxiety-related behaviour, c-Fos expression was used to map neuronal activation in the PVN in response to the mild emotional challenge of open arm exposure. As with the C57Bl/6N strain, Mg2+ deficiency increased anxiety-related behaviour in BALB/c mice which was reversed by diazepam treatment as indicated by significant dietary and drug effects in the measures “percentage of entries into the anxiogenic distal part of the open arm” (diet: F1,35 = 12.615, P < 0.01; drug: F1,35 = 15.359, P < 0.001, Table 4, Fig. 4A) and “total distance travelled” (diet: F1,35 = 6.120, P < 0.05; drug: F1,36 = 33.519, P < 0.001; Table 4). Furthermore, diazepam significantly affected the percentage of time spent in the distal compartment (F1,35 = 10.352, P < 0.01) (Table 4).


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

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

Effect of Mg2+ deficiency and diazepam treatment (1 mg/kg, i.p.) on behaviour and c-Fos expression in the paraventricular hypothalamic nucleus (PVN) of BALB/c mice following exposure to the open arm of an elevated plus maze. A. In mice fed a Mg2+ restricted diet the anxiety-related behaviour was elevated as indicated by the number of entries into the (anxiogenic) distal compartment of the open arm. Treatment with diazepam normalised this anxious phenotype. B. Compared with vehicle-treated controls, c-Fos induction was increased in the magnocellular portion of the PVN in Mg2+ deficient mice and was reversed by diazepam treatment. C. Representative photograph (scale bar = 100 μm) showing delineation of the PVN regions analysed with the help of a mouse brain atlas (Paxinos and Franklin, 2001). D. High magnification photograph showing c-Fos-positive cells in the magnocellular portion of the PVN in all experimental groups. Data represent mean ± SEM. n = 10 per experimental group. *P < 0.05, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for diazepam vs. vehicle. 3V: third ventricle; DZP: diazepam; magno: magnocellular portion of the PVN; parvo: parvocellular portion of the PVN; V: vehicle.
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fig4: Effect of Mg2+ deficiency and diazepam treatment (1 mg/kg, i.p.) on behaviour and c-Fos expression in the paraventricular hypothalamic nucleus (PVN) of BALB/c mice following exposure to the open arm of an elevated plus maze. A. In mice fed a Mg2+ restricted diet the anxiety-related behaviour was elevated as indicated by the number of entries into the (anxiogenic) distal compartment of the open arm. Treatment with diazepam normalised this anxious phenotype. B. Compared with vehicle-treated controls, c-Fos induction was increased in the magnocellular portion of the PVN in Mg2+ deficient mice and was reversed by diazepam treatment. C. Representative photograph (scale bar = 100 μm) showing delineation of the PVN regions analysed with the help of a mouse brain atlas (Paxinos and Franklin, 2001). D. High magnification photograph showing c-Fos-positive cells in the magnocellular portion of the PVN in all experimental groups. Data represent mean ± SEM. n = 10 per experimental group. *P < 0.05, ***P < 0.001 for Mg2+ deficient vs. control mice, ###P < 0.001 for diazepam vs. vehicle. 3V: third ventricle; DZP: diazepam; magno: magnocellular portion of the PVN; parvo: parvocellular portion of the PVN; V: vehicle.
Mentions: In an attempt to gain additional evidence for a possible functional relevance of increased PVN prepro-CRH mRNA expression in the Mg2+ deficiency-induced enhanced anxiety-related behaviour, c-Fos expression was used to map neuronal activation in the PVN in response to the mild emotional challenge of open arm exposure. As with the C57Bl/6N strain, Mg2+ deficiency increased anxiety-related behaviour in BALB/c mice which was reversed by diazepam treatment as indicated by significant dietary and drug effects in the measures “percentage of entries into the anxiogenic distal part of the open arm” (diet: F1,35 = 12.615, P < 0.01; drug: F1,35 = 15.359, P < 0.001, Table 4, Fig. 4A) and “total distance travelled” (diet: F1,35 = 6.120, P < 0.05; drug: F1,36 = 33.519, P < 0.001; Table 4). Furthermore, diazepam significantly affected the percentage of time spent in the distal compartment (F1,35 = 10.352, P < 0.01) (Table 4).

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