Low [3H]Cytochalasin B Binding in the Cerebral Cortex of Newborn Rat

Authors

  • Anne M. Morin,

    Corresponding author
    1. Veterans Administration Medical Center, Sepulveda, and Department of Neurology and Brain Research Institute, University of California School of Medicine, Los Angeles, California, U.S.A.
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  • Barney E. Dwyer,

    1. Veterans Administration Medical Center, Sepulveda, and Department of Neurology and Brain Research Institute, University of California School of Medicine, Los Angeles, California, U.S.A.
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  • Denson G. Fujikawa,

    1. Veterans Administration Medical Center, Sepulveda, and Department of Neurology and Brain Research Institute, University of California School of Medicine, Los Angeles, California, U.S.A.
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  • Claude G. Wasterlain

    1. Veterans Administration Medical Center, Sepulveda, and Department of Neurology and Brain Research Institute, University of California School of Medicine, Los Angeles, California, U.S.A.
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Address correspondence and reprint requests to Dr. A. M. Morin at Neurology Research Laboratory (11 1N1), Veterans Administration Medical Center, 16111 Plummer St., Sepulveda, CA 91343, U.S.A.

Abstract

The concentrations of glucose transporter in the cerebral cortex and brainstem of neonatal (4–7 days old) and adult rats were measured using [3H]cytochalasin B binding. There was significantly lower binding in neonatal cortex (1.9 ± 0.7 pmol/mg protein) compared to adult (8.9 ± 2.5 pmol/mg protein). Scatchard analysis indicates this difference is due to a lower Bmax (neonate, 9.7 pmol/mg protein; adult, 18.6 ± 1.3 pmol/mg protein). Measurement of [3H]cytochalasin B binding in microvessels prepared from cortex of adult (28.1 ± 3.5 pmol/mg protein) and neonate (12.8 ± 1.9 pmol/mg protein) indicates a lower binding in the microvasculature of neonates, whereas no such difference was seen in the binding in microvessels prepared from adult and neonatal brainstem (adult, 11.8 ± 2.3 pmol/mg protein; neonate, 9.4 ± 2.7 pmol/mg protein). In both adult and neonate brain, there is an enrichment of glucose transporters in the microvasculature.

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