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Pre-natal amino acid transport inhibition: long term influences on behavior and protein metabolism

S Samuels, C T Randt, I Fish

    Pharmacology, Biochemistry, and Behavior
    |January 1, 1986
    PubMed

    Insights

    Prenatal exposure to enzyme inhibitors altered motor behavior and brain amino acid uptake in young mice. These findings suggest long-term consequences of interfering with blood-brain amino acid transport during development.

    Area of Science:

    • Neuroscience
    • Developmental Biology
    • Biochemistry

    Background:

    • Blood-brain barrier (BBB) transport of large-neutral amino acids is crucial for normal brain development.
    • Disruptions in amino acid transport during critical developmental windows can have lasting effects.

    Purpose of the Study:

    • To investigate the long-term effects of in utero exposure to enzyme inhibitors on amino acid transport and behavior in mice.
    • To explore potential links between altered amino acid transport and neurodevelopmental outcomes.

    Main Methods:

    • DBA/2J mice were exposed gestationally (days 15-18) to L-methionine-RS-sulfoximine or 2-imidazolidone-4-carboxylic acid.
    • Motor behavior was assessed in young mice (40-42 days old).
    • Brain entry and incorporation of 14C-valine were measured up to 80 days of age.

    Main Results:

    • Mice exposed in utero exhibited persistent alterations in motor behavior compared to saline controls.
    • Differences in 14C-valine entry and incorporation into the brain were observed up to 80 days of age.
    • These effects indicate long-term consequences of developmental interference with amino acid transport.

    Conclusions:

    • Interference with blood-brain amino acid transport during critical in utero development has persistent neurobehavioral and neurochemical consequences.
    • These findings may offer insights into human conditions like maternal phenylketonuria, where amino acid metabolism is altered.
    • The study highlights the vulnerability of the developing brain to disruptions in nutrient transport.

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