Ontogeny of the calcium binding protein calbindin D-28k in the rat nervous system

1987 ◽  
Vol 177 (1) ◽  
pp. 15-28 ◽  
Author(s):  
Susann Enderlin ◽  
A. W. Norman ◽  
Marco R. Celio
Keyword(s):  
Nervous System ◽  
Calcium Binding ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Calbindin D

Differential expression of the EF-hand calcium-binding protein calsensin in the central nervous system of hirudinid leeches

1996 ◽  
Vol 286 (3) ◽  
pp. 357-364 ◽  
Author(s):  
Mark Veldman ◽  
Yueqiao Huang ◽  
John Jellies ◽  
Kristen M. Johansen ◽  
Jørgen Johansen
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Differential Expression ◽  
Calcium Binding ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Ef Hand ◽  
The Central Nervous System

Endocrine control of plasma concentrations of calcium-binding protein in the pig

1987 ◽  
Vol 115 (1) ◽  
pp. 121-128
Author(s):  
E. M. W. Maunder ◽  
A. V. Pillay ◽  
A. D. Care
Keyword(s):  
Calcium Binding ◽  
Binding Protein ◽  
Plasma Concentrations ◽  
Significant Rise ◽  
Calcium Binding Protein ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Endocrine Control ◽  
Adrenergic Blocker ◽  
Calbindin D

ABSTRACT The aetiology of the rise in plasma calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP), following insulin-induced hypoglycaemia, was studied in the pig. ACTH led to a rise in plasma concentrations of both CaBP and cortisol. Metyrapone, which blocks cortisol synthesis, abolished the increases in plasma concentrations of CaBP and cortisol normally observed in response to insulin-induced hypoglycaemia. However, there was no significant rise in plasma concentrations of CaBP in response to pharmacological or physiological doses of cortisol. Injection of clonidine, an α2-adrenergic agonist, led to a rise in plasma concentrations of CaBP, whereas phenylephrine, an α1-adrenergic agonist, tended to exert an inhibitory effect. Also, administration of phentolamine (an α-adrenergic blocker) before injection of insulin abolished the usual increase in plasma concentrations of CaBP, whereas propranolol (a β-adrenergic blocker) enhanced the normal increase in plasma concentrations of CaBP in response to insulin-induced hypoglycaemia. Isoproterenol, a β-adrenergic agonist, was without effect on plasma CaBP. Neither GH nor glucagon appear to be involved in the rise in plasma CaBP following insulin-induced hypoglycaemia. Although atropine abolished the effect of acute hypoglycaemia on plasma CaBP, carbamylcholine was without effect on plasma CaBP concentration. It is concluded that the increases in plasma CaBP induced by either ACTH or α2-adrenergic stimulation may be interrelated since the administration of ACTH can lead to raised plasma concentrations of catecholamines. J. Endocr. (1987) 115, 121–128

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