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Reduced intracellular mobility underlies manganese relaxivity in mouse brain in vivo: MRI at 2.35 and 9.4 T

Takashi Watanabe1, Jens Frahm, Thomas Michaelis

  • 1Biomedizinische NMR Forschungs GmbH am Max-Planck-Institut für Biophysikalische Chemie, 37070, Göttingen, Germany, twatana@gwdg.de.

Brain Structure & Function
|March 22, 2014
PubMed

Insights

Manganese ions in mouse brains show reduced mobility in vivo, impacting MRI contrast. This effect is more pronounced at lower magnetic field strengths, suggesting intracellular localization and binding.

Area of Science:

  • Neuroimaging
  • Biophysics
  • Magnetic Resonance Imaging (MRI)

Background:

  • Paramagnetic contrast agents like manganese ions (Mn2+) alter MRI signal.
  • Understanding the in vivo behavior of contrast agents is crucial for accurate imaging.
  • Magnetic field strength can influence relaxivity, affecting image contrast.

Purpose of the Study:

  • To investigate the in vivo longitudinal relaxivity of manganese ions in mouse brains.
  • To determine the influence of magnetic field strength on manganese-induced MRI contrast.
  • To explore the localization and mobility of manganese ions within brain tissue.

Main Methods:

  • T1-weighted MRI was performed at 2.35 T and 9.4 T magnetic field strengths.
  • Manganese chloride was administered systemically, and gadolinium-DTPA (Gd-DTPA) intraventricularly.
  • Longitudinal relaxation rates (∆R1) and relaxivity ratios were calculated and compared.

Main Results:

  • Manganese-induced ∆R1 was significantly higher at 2.35 T than 9.4 T, with ratios ranging from 2.4 to 4.4.
  • Gd-DTPA showed no significant field strength dependence in ∆R1 (ratios 1.0-1.1).
  • Manganese relaxivity in aqueous solution also showed no field strength dependence.

Conclusions:

  • The field strength dependence of manganese relaxivity indicates reduced intracellular mobility in vivo.
  • Manganese likely localizes intracellularly, potentially binding to macromolecules or confined in viscous compartments.
  • Magnetization transfer and slow postmortem manganese release further support intracellular localization.

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