Elsevier

Brain Research

Volume 747, Issue 2, 7 February 1997, Pages 195-206
Brain Research

Research report
Effects of maternal oral administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain

https://doi.org/10.1016/S0006-8993(96)01181-XGet rights and content

Abstract

Monosodium glutamate (MSG) was shown to penetrate placental barrier and to distribute to embryonic tissues using [3H]glutamic acid ([3H]Glu) as a tracer. However, the distribution is not even; the uptake of MSG in the fetal brain was twice as great as that in the maternal brain in Kunming mice. Other maternal mice were given per os MSG (2.5 mg/g or 4.0 mg/g body weight) at 17–21 days of pregnancy, and their offspring behaviors studied. The results showed that maternal oral administration of MSG at a late stage of pregnancy decreased the threshold of convulsion in the litters at 10 days of age. Y-maze discrimination learning was significantly impaired in the 60-day-old filial mice. On the other hand, no significant difference in spatial learning or tail flick latency was measured between the experimental animals and the controls. The filial mice of MSG-treated mothers could either not grasp a rope tightly, or grasped the rope tightly but could not crawl along the rope at the beginning of the training. However, such mice, after training, could grasp and crawl along the rope as well as controls. Obvious neuronal damage was not detected in the periventricular organs or the hypothalamus under a light microscope. The rate of weight gain for experimental animals was greater than for controls throughout the period from 20 to 90 days. Mating of treated males with treated females resulted in pregnancies and normal offspring, indicating that oral administration of MSG at a late stage of pregnancy did not affected the reproductive capacity of the offspring. The possible differences and relationship between MSG-induced damage to developing human and rodent brain are discussed.

References (45)

  • J.Y. Cheung et al.

    Calcium and ischemic injury

    New Engl. J. Med.

    (1986)
  • D.W. Choi

    Ionic dependence of glutamate neurotoxicity in cortical cell culture

    J. Neurosci.

    (1987)
  • J.W. Ferkany et al.

    Dextromethorphan inhibits NMDA-induced convulsions

    Eur. J. Pharmacol.

    (1987)
  • J. Gao et al.

    Transplacental neurotoxic effects of monosodium glutamate on structures and functions of specific brain areas of filial mice

    Acta Physiol. Sin.

    (1994)
  • M. Inouye et al.

    Brain lesions in mouse infants and fetuses induced by monosodium L. aspartate

    Congen. Anomal.

    (1973)
  • H. Lodish et al.

    Molecular Cell Biology

  • D.R. Lucas et al.

    The toxic effect of sodium L-glutamate on the inner layers of the retina

    AMA Arch. Ophthalmol.

    (1957)
  • A.B. MacDermott et al.

    NMDA-receptor activation increases cytoplasmic calcium concentration in cultured spinal cord neurons

    Nature

    (1986)
  • M.L. Mayer et al.

    Permeation and block of N-methyl-D-aspartic acid receptor channels by divalent cations in mouse cultured central neurons

    J. Physiol.

    (1987)
  • B.S. Meldrum et al.

    Excitatory amino acid neurotoxicity and neurodegenerative disease

    Trends. Pharmacol. Sci.

    (1990)
  • J.W. Olney

    Brain lesions, obesity and other disturbances in mice treated with monosodium glutamate

    Sciences

    (1969)
  • J.W. Olney

    Glutamate-induced neuronal necrosis in the infant mouse hypothalamus, an electron microscopic study

    J. Neuropathol. Exp. Neurol.

    (1971)
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