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Peripheral Infusion of Insulin-Like Growth Factor-I Increases the Number of Newborn Oligodendrocytes in the Cerebral Cortex of Adult Hypophysectomized Rats

Department of Internal Medicine (N.D.Å., J.I.), Research Centre of Endocrinology and Metabolism, Institute of Medicine, Center of Brain Repair and Rehabilitation (N.D.Å., U.E.J., M.A.I.Å., N.A.K.H., J.L., C.B., M.F.A., P.S.E.), Institute for Clinical Neuroscience and Physiology, and Wallenberg Laboratory for Cardiovascular Research (J.O.), Göteborg University, SE-413 45 Göteborg, Sweden

Address all correspondence and requests for reprints to: Dr. N. David Åberg, Department of Internal Medicine, Research Center of Endocrinology and Metabolism, Sahlgrenska University Hospital, Göteborg University, Gröna Stråket 8, SE-413 45 Göteborg, Sweden. E-mail: david.aberg{at}medic.gu.se.

We have previously shown that recombinant human (rh) IGF-I induces cell proliferation and neurogenesis in the hippocampus of hypophysectomized rats. In the current investigation, we determined the effects of rhIGF-I on proliferation and differentiation in the cerebral cortex. Adult hypophysectomized rats were injected with bromodeoxyuridine (BrdU) to label newborn cells (once a day for the first 5 d), and rhIGF-I was administered peripherally for 6 or 20 d. In the cerebral cortex, the number of BrdU-labeled cells increased after 20 d but not after 6 d of rhIGF-I infusion. This suggests that rhIGF-I enhances the survival of newborn cells in the cerebral cortex. Using BrdU labeling combined with the oligodendrocyte-specific markers myelin basic protein and 2',3'-cyclic nucleotide 3'-phosphodiesterase, we demonstrated an increase in oligodendrogenesis in the cerebral cortex. The total amount of myelin basic protein and 2',3'-cyclic nucleotide 3'-phosphodiesterase was also increased on Western blots of homogenates of the cerebral cortex, confirming the immunohistochemical findings. Also, we observed an increase in the number of capillary-associated BrdU-positive cells, although total capillary area was not increased. rhIGF-I treatment did not affect cortical astrogliogenesis and neurogenesis was not observed. The ability of rhIGF-I to induce cortical oligodendrogenesis may have implications for the regenerative potential of the cortex.

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