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
Hauptverfasser: Rabié, A., Bréhier, A., Intrator, S., Clavel, M.C., Parkes, C.O., Legrand, C., Thomasset, M.
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container_end_page 265
container_issue 2
container_start_page 253
container_title Brain research
container_volume 29
creator Rabié, A.
Bréhier, A.
Intrator, S.
Clavel, M.C.
Parkes, C.O.
Legrand, C.
Thomasset, M.
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.
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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. 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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><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation</subject><subject>Cell Movement</subject><subject>cerebellum</subject><subject>Cerebellum - growth &amp; 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. 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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. 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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. 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source MEDLINE; Access via ScienceDirect (Elsevier); Alma/SFX Local Collection
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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