Artigo Revisado por pares

Differential effect of thyroid hormone deficiency on the growth of calretinin-expressing neurons in rat spinal cord and dorsal root ganglia

2000; Wiley; Volume: 426; Issue: 4 Linguagem: Inglês

10.1002/1096-9861(20001030)426

ISSN

1096-9861

Autores

Ibtissam Barakat‐Walter, Rudolf Kraftsik, Thierry Küntzer, Julien Bogousslavsky, Pierre J. Magistretti,

Tópico(s)

Cardiovascular, Neuropeptides, and Oxidative Stress Research

Resumo

Journal of Comparative NeurologyVolume 426, Issue 4 p. 519-533 Article Differential effect of thyroid hormone deficiency on the growth of calretinin–expressing neurons in rat spinal cord and dorsal root ganglia Ibtissam Barakat-Walter, Corresponding Author Ibtissam Barakat-Walter [email protected] Institute of Cell Biology and Morphology (IBCM), Medical School, University of Lausanne, 1005 Lausanne, Switzerland Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandCHUV-Laboratoire de Recherche Neurologique, BH, 19, Rue du Bugnon 46, 1011 Lausanne, SwitzerlandSearch for more papers by this authorRudolf Kraftsik, Rudolf Kraftsik Institute of Cell Biology and Morphology (IBCM), Medical School, University of Lausanne, 1005 Lausanne, SwitzerlandSearch for more papers by this authorThierry Kuntzer, Thierry Kuntzer Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandSearch for more papers by this authorJulien Bogousslavsky, Julien Bogousslavsky Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandSearch for more papers by this authorPierre Magistretti, Pierre Magistretti Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandSearch for more papers by this author Ibtissam Barakat-Walter, Corresponding Author Ibtissam Barakat-Walter [email protected] Institute of Cell Biology and Morphology (IBCM), Medical School, University of Lausanne, 1005 Lausanne, Switzerland Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandCHUV-Laboratoire de Recherche Neurologique, BH, 19, Rue du Bugnon 46, 1011 Lausanne, SwitzerlandSearch for more papers by this authorRudolf Kraftsik, Rudolf Kraftsik Institute of Cell Biology and Morphology (IBCM), Medical School, University of Lausanne, 1005 Lausanne, SwitzerlandSearch for more papers by this authorThierry Kuntzer, Thierry Kuntzer Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandSearch for more papers by this authorJulien Bogousslavsky, Julien Bogousslavsky Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandSearch for more papers by this authorPierre Magistretti, Pierre Magistretti Laboratory of Neurology Research, University Hospital of Lausanne, 1011 Lausanne, SwitzerlandSearch for more papers by this author First published: 19 October 2000 https://doi.org/10.1002/1096-9861(20001030)426:4 3.0.CO;2-6Citations: 11Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract The development of spinal cord or dorsal root ganglia neurons expressing calretinin (CR) was studied in thyroid hormone-deficient rats. Immunocytochemical and morphometric analyses showed that the hypothyroidism induced a significant decrease in the number and size of immunoreactive neurons in the spinal cord, as well as stunted growth and arborization of the axons and dendrites. These alterations were observed at different embryonic ages and persisted during the whole postnatal life. In adult hypothyroid rats, the mean number of CR-positive neurons per spinal cord section (31.2 ± 2.3 in laminae I and II and 30.5 ± 5.5 in laminae III–X) was significantly decreased (P < 0.001 and P = 0.024, respectively) compared with adult normal rats (68.7 ± 8.9 and 50.0 ± 11.0, respectively). In the peripheral nervous system, hypothyroidism altered the growth of sensory neurons expressing CR protein mainly during embryonic life. In comparison with normal rats, hypothyroid embryonic animals showed not only reduced cell size but also a significantly decreased percentage of CR-positive neurons (6.6 ± 0.9% in normal, 2.1 ± 0.3% in hypothyroid rats, P < 0.001). In contrast, although the size of neurons was reduced in hypothyroid young and adult rats, there was no reduction in the percentage of CR-positive neurons. These results showed that thyroid hormone deficiency altered differentially the development of neurons expressing CR protein in the central and peripheral nervous systems. This suggests that central and peripheral neurons are heterogeneous in their sensitivity to thyroid hormone. J. Comp. Neurol. 426:519–533, 2000. © 2000 Wiley-Liss, Inc. LITERATURE CITED Aleyamma PT, Nathaniel EJH. 1992. 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