title: Characterization of calcium accumulation in the brain of rats administered orally calcium: the significance of energy-dependent mechanism.
abstract: The characterization of calcium accumulation in the brain of rats administered orally calcium chloride solution was investigated. Rats received a single oral administration of calcium (15-50 mg/100 g body weight), and they were sacrificed by bleeding between 15 and 120 min after the administration. The administration of calcium (50 mg/100 g) produced a significant increase in serum calcium concentration and a corresponding elevation of brain calcium content, indicating that the transport of calcium into the brain is associated with the elevation of serum calcium levels. The increase in brain calcium content by calcium administration was not appreciably altered by the pretreatment with Ca2+ channel blockers (verapamil or diltiazem with the doses of 1.5 and 3.0 mg/100 g). In thyroparathyroidectomized rats, the administration of calcium (50 mg/100 g) caused a significant increase in brain calcium content, indicating that calcium-regulating hormones do not participate in the brain calcium transport. Now, brain calcium content was clearly elevated by fasting (overnight), although serum calcium level was not significantly altered. Calcium administration to fasted rats induced a further elevation of brain calcium content as compared with that of control (fasted) rats. The fasting-induced increase in brain calcium content was appreciably restored by refeeding. This restoration was also seen by the oral administration of glucose (0.4 g/100 g) to fasted rats. The present study demonstrates that serum calcium is transported to brain, and that the increased brain calcium is released promptly. The release of calcium from brain may be involved in energy metabolism, and this release may be weakened by the reduction of glucose supply into brain. The finding suggests a physiological significance of energy-dependent mechanism in the regulation of brain calcium.
authors.affiliation: Laboratory of Endocrinology and Molecular Metabolism, Graduate School of Nutritional Sciences, University of Shizuoka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Hanahisa
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
mesh_terms: D000818:Animals; D001692:Biological Transport; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002116:Calcitonin / Q000378:metabolism; D002118:Calcium / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D004734:Energy Metabolism / Q000502:physiology; D005215:Fasting / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D008297:Male; D010280:Parathyroid Glands / Q000502:physiology; D010281:Parathyroid Hormone / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013965:Thyroidectomy; D014700:Verapamil / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D010281:Parathyroid Hormone; D002116:Calcitonin; D014700:Verapamil; D004110:Diltiazem; D005947:Glucose; D002118:Calcium