Abstract
There is evidence that magnesium (Mg2þ) deficiency may causally be involved in stress responses and modulation of emotionality. It has also been hypothesized that geneticallybased low blood Mg2þ levels may account for stress
susceptibility, probably via modulation of the release of
adrenocorticotropic hormone (ACTH) and, thus, activity of the hypothalamic–pituitary–adrenocortical (HPA) axis. We aim at evaluating whether: (1) differences in anxiety-related behaviour in inbred mouse strains correspond to plasma Mg2þ concentration; and (2) whether systemic treatment with Mg2þ
abolishes possibly corresponding strain differences. Furthermore, the long-term goal of our project is to evaluate the genetic background for anxiety-modulating capabilities of Mg2þ in mice. Therefore, we have chosen to investigate the A/J and C57BL/6J strains, which are the parental strains
of the commercially available set of chromosome substitution strains (CSSs) that can be used for further genetic analysis. In the experiment reported here, BALB/c mice are used as an additional control group, since this strain has been reported extensively to be characterized by high innate anxiety. All three inbred strains are behaviourally tested in the modified hole board (mHB), allowing for the parallel evaluation of a variety of motivational systems potentially involved in
emotionality. One week after initial testing, the animals are re-tested, after having received either vehicle or magnesium sulphate. Subsequently to behavioural testing, blood is sampled via tail incision to allow for the analysis of
plasma Mg2þ concentrations as well as stress hormone responses. The first pilot studies in our lab have shown that the two CSS parental strains (i.e. A/J and C57BL/6) differ in a variety of behavioural parameters, including anxietyrelated measures, which corresponds with differences in plasma Mg2þ levels. These results emphasize the hypothesized, and possibly causal, association between magnesium status and emotionality.
susceptibility, probably via modulation of the release of
adrenocorticotropic hormone (ACTH) and, thus, activity of the hypothalamic–pituitary–adrenocortical (HPA) axis. We aim at evaluating whether: (1) differences in anxiety-related behaviour in inbred mouse strains correspond to plasma Mg2þ concentration; and (2) whether systemic treatment with Mg2þ
abolishes possibly corresponding strain differences. Furthermore, the long-term goal of our project is to evaluate the genetic background for anxiety-modulating capabilities of Mg2þ in mice. Therefore, we have chosen to investigate the A/J and C57BL/6J strains, which are the parental strains
of the commercially available set of chromosome substitution strains (CSSs) that can be used for further genetic analysis. In the experiment reported here, BALB/c mice are used as an additional control group, since this strain has been reported extensively to be characterized by high innate anxiety. All three inbred strains are behaviourally tested in the modified hole board (mHB), allowing for the parallel evaluation of a variety of motivational systems potentially involved in
emotionality. One week after initial testing, the animals are re-tested, after having received either vehicle or magnesium sulphate. Subsequently to behavioural testing, blood is sampled via tail incision to allow for the analysis of
plasma Mg2þ concentrations as well as stress hormone responses. The first pilot studies in our lab have shown that the two CSS parental strains (i.e. A/J and C57BL/6) differ in a variety of behavioural parameters, including anxietyrelated measures, which corresponds with differences in plasma Mg2þ levels. These results emphasize the hypothesized, and possibly causal, association between magnesium status and emotionality.
Original language | English |
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Pages | 37-37 |
Number of pages | 1 |
Publication status | Published - 1 Sept 2005 |
Event | 11th Biennial EBPS Meeting - Barcelona, Spain Duration: 9 Sept 2005 → 12 Sept 2005 |
Conference
Conference | 11th Biennial EBPS Meeting |
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Country/Territory | Spain |
City | Barcelona |
Period | 9/09/05 → 12/09/05 |