Thyroid state and cholecalcin (calcium-binding protein) in cerebellum of the developing rat
Cholecalcin (28,000 Da, vitamin D-dependent calcium-binding protein) is a marker of Purkinje cell development in the rat cerebellum from embryonic day 17 when these cells can first be distinguished. Specific antibodies raised against human cerebellar or rat renal cholecalcin were used in an immunocy...
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Veröffentlicht in: | Brain research 1986-10, Vol.29 (2), p.253-265 |
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description | Cholecalcin (28,000 Da, vitamin D-dependent calcium-binding protein) is a marker of Purkinje cell development in the rat cerebellum from embryonic day 17 when these cells can first be distinguished. Specific antibodies raised against human cerebellar or rat renal cholecalcin were used in an immunocytochemical and quantitative study in altered thyroid states. The immunocytochemical staining was qualitatively similar in both normal and hypothyroid animals but clearly demonstrated the slowing of Purkinje cell development resulting from the lack of thyroxine. This effect was also reflected in quantitative studies which showed that the total cholecalcin per cerebellum was lower in thyroid-deficient rats. However, there was, in these animals, no specific reduction in cholecalcin level. Moreover, the response to thyroxine treatment indicated that the synthesis of cholecalcin occurred later and slower than that of the majority of cerebellar proteins and even after other more complex mechanisms of cerebellar cortex development (such as neurite outgrowth) have been induced. Thus, cholecalcin synthesis does not appear particularly sensitive to thyroid hormone level but might rather follow the increase in cell size induced by the hormone. |
doi_str_mv | 10.1016/0165-3806(86)90101-X |
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Specific antibodies raised against human cerebellar or rat renal cholecalcin were used in an immunocytochemical and quantitative study in altered thyroid states. The immunocytochemical staining was qualitatively similar in both normal and hypothyroid animals but clearly demonstrated the slowing of Purkinje cell development resulting from the lack of thyroxine. This effect was also reflected in quantitative studies which showed that the total cholecalcin per cerebellum was lower in thyroid-deficient rats. However, there was, in these animals, no specific reduction in cholecalcin level. Moreover, the response to thyroxine treatment indicated that the synthesis of cholecalcin occurred later and slower than that of the majority of cerebellar proteins and even after other more complex mechanisms of cerebellar cortex development (such as neurite outgrowth) have been induced. Thus, cholecalcin synthesis does not appear particularly sensitive to thyroid hormone level but might rather follow the increase in cell size induced by the hormone.</description><identifier>ISSN: 0165-3806</identifier><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/0165-3806(86)90101-X</identifier><identifier>PMID: 3768729</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Cell Differentiation ; Cell Movement ; cerebellum ; Cerebellum - growth & development ; cholecalcin (calcium-binding protein) ; Congenital Hypothyroidism ; developing rat ; Fundamental and applied biological sciences. Psychology ; Hypothyroidism - physiopathology ; Microscopy, Electron ; Organ Size ; Purkinje cell ; Rats ; Rats, Inbred Strains ; S100 Calcium Binding Protein G - metabolism ; thyroid deficiency ; Thyroid Hormones - physiology ; Thyroid. Parathyroid. Ultimobranchial body ; thyroxine effects ; Vertebrates: endocrinology</subject><ispartof>Brain research, 1986-10, Vol.29 (2), p.253-265</ispartof><rights>1986</rights><rights>1987 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-cba038c85d27c93897f867fe37be7c9873cba1f78f93d2232a9b49a5ac37f17b3</citedby><cites>FETCH-LOGICAL-c449t-cba038c85d27c93897f867fe37be7c9873cba1f78f93d2232a9b49a5ac37f17b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8038416$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3768729$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rabié, A.</creatorcontrib><creatorcontrib>Bréhier, A.</creatorcontrib><creatorcontrib>Intrator, S.</creatorcontrib><creatorcontrib>Clavel, M.C.</creatorcontrib><creatorcontrib>Parkes, C.O.</creatorcontrib><creatorcontrib>Legrand, C.</creatorcontrib><creatorcontrib>Thomasset, M.</creatorcontrib><title>Thyroid state and cholecalcin (calcium-binding protein) in cerebellum of the developing rat</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Cholecalcin (28,000 Da, vitamin D-dependent calcium-binding protein) is a marker of Purkinje cell development in the rat cerebellum from embryonic day 17 when these cells can first be distinguished. Specific antibodies raised against human cerebellar or rat renal cholecalcin were used in an immunocytochemical and quantitative study in altered thyroid states. The immunocytochemical staining was qualitatively similar in both normal and hypothyroid animals but clearly demonstrated the slowing of Purkinje cell development resulting from the lack of thyroxine. This effect was also reflected in quantitative studies which showed that the total cholecalcin per cerebellum was lower in thyroid-deficient rats. However, there was, in these animals, no specific reduction in cholecalcin level. Moreover, the response to thyroxine treatment indicated that the synthesis of cholecalcin occurred later and slower than that of the majority of cerebellar proteins and even after other more complex mechanisms of cerebellar cortex development (such as neurite outgrowth) have been induced. Thus, cholecalcin synthesis does not appear particularly sensitive to thyroid hormone level but might rather follow the increase in cell size induced by the hormone.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation</subject><subject>Cell Movement</subject><subject>cerebellum</subject><subject>Cerebellum - growth & development</subject><subject>cholecalcin (calcium-binding protein)</subject><subject>Congenital Hypothyroidism</subject><subject>developing rat</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hypothyroidism - physiopathology</subject><subject>Microscopy, Electron</subject><subject>Organ Size</subject><subject>Purkinje cell</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>S100 Calcium Binding Protein G - metabolism</subject><subject>thyroid deficiency</subject><subject>Thyroid Hormones - physiology</subject><subject>Thyroid. Parathyroid. Ultimobranchial body</subject><subject>thyroxine effects</subject><subject>Vertebrates: endocrinology</subject><issn>0165-3806</issn><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMotX78A4UcROxhNdlsN8lFEPELBC8KBQ8hm0xsZD9qsiv035va0qMehoF5nxmGB6ETSi4poeVVqmnGBCkvRDmRJM2y2Q4aU8HzrMwLsovGW2QfHcT4SQihTNARGjFeJkyO0fvrfBk6b3HsdQ9YtxabeVeD0bXxLb747UOTVb61vv3Ai9D14NsJTqGBABXU9dDgzuF-DtjCN9TdYgUG3R-hPafrCMebfoje7u9ebx-z55eHp9ub58wUhewzU2nChBFTm3MjmZDciZI7YLyCNBCcJYI6LpxkNs9ZrmVVSD3VhnFHecUO0fn6bnrua4DYq8ZHkx7TLXRDVJwTISWl_4K04HmRS57AYg2a0MUYwKlF8I0OS0WJWslXK7NqZVaJUv3KV7O0drq5P1QN2O3SxnbKzza5jkmsC7o1Pm4xkTQUtEzY9RqDJO3bQ1DReGgNWB_A9Mp2_u8_fgATSKCC</recordid><startdate>19861001</startdate><enddate>19861001</enddate><creator>Rabié, A.</creator><creator>Bréhier, A.</creator><creator>Intrator, S.</creator><creator>Clavel, M.C.</creator><creator>Parkes, C.O.</creator><creator>Legrand, C.</creator><creator>Thomasset, M.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19861001</creationdate><title>Thyroid state and cholecalcin (calcium-binding protein) in cerebellum of the developing rat</title><author>Rabié, A. ; Bréhier, A. ; Intrator, S. ; Clavel, M.C. ; Parkes, C.O. ; Legrand, C. ; Thomasset, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-cba038c85d27c93897f867fe37be7c9873cba1f78f93d2232a9b49a5ac37f17b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation</topic><topic>Cell Movement</topic><topic>cerebellum</topic><topic>Cerebellum - growth & development</topic><topic>cholecalcin (calcium-binding protein)</topic><topic>Congenital Hypothyroidism</topic><topic>developing rat</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hypothyroidism - physiopathology</topic><topic>Microscopy, Electron</topic><topic>Organ Size</topic><topic>Purkinje cell</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>S100 Calcium Binding Protein G - metabolism</topic><topic>thyroid deficiency</topic><topic>Thyroid Hormones - physiology</topic><topic>Thyroid. Parathyroid. Ultimobranchial body</topic><topic>thyroxine effects</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rabié, A.</creatorcontrib><creatorcontrib>Bréhier, A.</creatorcontrib><creatorcontrib>Intrator, S.</creatorcontrib><creatorcontrib>Clavel, M.C.</creatorcontrib><creatorcontrib>Parkes, C.O.</creatorcontrib><creatorcontrib>Legrand, C.</creatorcontrib><creatorcontrib>Thomasset, M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rabié, A.</au><au>Bréhier, A.</au><au>Intrator, S.</au><au>Clavel, M.C.</au><au>Parkes, C.O.</au><au>Legrand, C.</au><au>Thomasset, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thyroid state and cholecalcin (calcium-binding protein) in cerebellum of the developing rat</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1986-10-01</date><risdate>1986</risdate><volume>29</volume><issue>2</issue><spage>253</spage><epage>265</epage><pages>253-265</pages><issn>0165-3806</issn><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Cholecalcin (28,000 Da, vitamin D-dependent calcium-binding protein) is a marker of Purkinje cell development in the rat cerebellum from embryonic day 17 when these cells can first be distinguished. Specific antibodies raised against human cerebellar or rat renal cholecalcin were used in an immunocytochemical and quantitative study in altered thyroid states. The immunocytochemical staining was qualitatively similar in both normal and hypothyroid animals but clearly demonstrated the slowing of Purkinje cell development resulting from the lack of thyroxine. This effect was also reflected in quantitative studies which showed that the total cholecalcin per cerebellum was lower in thyroid-deficient rats. However, there was, in these animals, no specific reduction in cholecalcin level. Moreover, the response to thyroxine treatment indicated that the synthesis of cholecalcin occurred later and slower than that of the majority of cerebellar proteins and even after other more complex mechanisms of cerebellar cortex development (such as neurite outgrowth) have been induced. Thus, cholecalcin synthesis does not appear particularly sensitive to thyroid hormone level but might rather follow the increase in cell size induced by the hormone.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>3768729</pmid><doi>10.1016/0165-3806(86)90101-X</doi><tpages>13</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Cell Differentiation Cell Movement cerebellum Cerebellum - growth & development cholecalcin (calcium-binding protein) Congenital Hypothyroidism developing rat Fundamental and applied biological sciences. Psychology Hypothyroidism - physiopathology Microscopy, Electron Organ Size Purkinje cell Rats Rats, Inbred Strains S100 Calcium Binding Protein G - metabolism thyroid deficiency Thyroid Hormones - physiology Thyroid. Parathyroid. Ultimobranchial body thyroxine effects Vertebrates: endocrinology |
title | Thyroid state and cholecalcin (calcium-binding protein) in cerebellum of the developing rat |
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