The Role of Growth Hormone in Neural Development

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Abstract

Growth hormone (GH) is integrally involved in the development of the central nervous system (CNS), as well as during its recovery from injury, two processes that share many similarities and may influence CNS functionality. This review discusses some of the most recent findings in the field and, in particular, the ontogeny, distribution, regulation and putative functions of GH and its receptor within the CNS, particularly during development. The relative roles of peripheral GH, acting in part through insulin-like growth factor-I, and of the autocrine/paracrine GH system within the brain are considered. The potential role of GH as a therapeutic agent to influence brain development and function is discussed.

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Leptin enters the brain by a saturable system independent of insulin

Weitao Huang, Jonathan B. Jaspan, Lawrence Maness … (1996)

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Igf1 gene disruption results in reduced brain size, CNS hypomyelination, and loss of hippocampal granule and striatal parvalbumin-containing neurons.

R. Widmer, F. Hefti, Francisco Valverde-Albacete … (1995)

Homozygous Igf1-/- mice at 2 months of age had reduced brain weights, with reductions evenly affecting all major brain areas. The gross morphology of the CNS was normal, but the size of white matter structures in brain and spinal cord was strongly reduced, owing to decreased numbers of axons and oligodendrocytes. Myelinated axons were more strongly reduced in number than unmyelinated axons. The volume of the dentate gyrus granule cell layer was reduced in excess of the decrease in brain weight. Among populations of calcium-binding protein-containing neurons, there was a selective reduction in the number of striatal parvalbumin-containing cells. Numbers of mesencephalic dopaminergic neurons, striatal and basal forebrain cholinergic neurons, and spinal cord motoneurons were unaffected. Cerebellar morphology was unaltered. Our findings suggest cell type- and region-specific functions for IGF-I and emphasize prominent roles in axon growth and maturation in CNS myelination.

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Early dexamethasone therapy in preterm infants: a follow-up study.

Julien Hsieh, J. C. Huang, Y-C Lien … (1998)

To study the outcome at 2-year corrected age of infants who participated in a double-blind controlled trial of early (<12 hours) dexamethasone therapy for the prevention of chronic lung disease (CLD). A total of 133 children (70 in the control group, 63 in the dexamethasone-treated group) who survived the initial study period and lived to 2 years of age were studied. All infants had birth weights of 500 to 1999 g and had severe respiratory distress syndrome requiring mechanical ventilation within 6 hours after birth. For infants in the treatment group, dexamethasone was started at a mean age of 8.1 hours and given 0.25 mg/kg every 12 hours for 1 week and then tapered off gradually over a 3-week period. The following variables were evaluated: interim medical history, socioeconomic background, physical growth, neurologic examinations, mental and psychomotor development index score (MDI and PDI), pulmonary function, electroencephalogram, and auditory and visual evoked potential. Infants in the control group tended to have a higher incidence of upper respiratory infection and rehospitalization than did the dexamethasone-treated group because of respiratory problems. Although there was no difference between the groups in somatic growth in girls, the dexamethasone-treated boys had significantly lower body weight and shorter height than the control boys (10.7 +/- 3.0 vs 11.9 +/- 2.0 kg; 84.9 +/- 5.7 vs 87.5 +/- 4.8 cm). The dexamethasone-treated group had a significantly higher incidence of neuromotor dysfunction (25/63 vs 12/70) than did the control group. The dexamethasone-treated infants also had a lower PDI score (79 +/- 26) than did the control group (87 +/- 23), but the difference was not statistically significant. Both groups were comparable in MDI, incidence of vision impairment, and auditory and visual evoked potential. Significant handicap, defined as severe neurologic defect and/or intellectual defect (MDI and/or PDI

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Author and article information

Journal

Journal ID (publisher-id): HRE

Journal ID (nlm-ta): Horm Res Paediatr

Journal ID (doi): 10.1159/issn.1663-2818

Title: Hormone Research in Paediatrics

Publisher: S. Karger AG

ISBN: 978-3-8055-8063-2

ISBN: 978-3-318-01309-2

ISSN (Print): 1663-2818

ISSN (Electronic): 1663-2826

Publication date Subscription-year: 2005

Publication date (Print): February 2006

Publication date (Electronic): 27 January 2006

Volume: 64

Issue: Suppl 3

Pages: 66-72

Affiliations

Liggins Institute, Faculty of Medicine and Health Sciences, University of Auckland, Auckland, New Zealand

Article

Publisher ID: 89320 Other ID: Horm Res 2005;64:66–72

DOI: 10.1159/000089320

PubMed ID: 16439847

SO-VID: 53cd7684-4919-444d-89e4-b49ac4a8a68e

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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The Role of Growth Hormone in Neural Development

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Abstract

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Karger: Endocrinology

Most cited references 59

Leptin enters the brain by a saturable system independent of insulin

Igf1 gene disruption results in reduced brain size, CNS hypomyelination, and loss of hippocampal granule and striatal parvalbumin-containing neurons.

Early dexamethasone therapy in preterm infants: a follow-up study.

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