Hanahisa Y, Yamaguchi M
Laboratory of Endocrinology and Molecular Metabolism, Graduate School of Nutritional Sciences, University of Shizuoka, Japan.
Mol Cell Biochem. 1996 May 10;158(1):1-7. doi: 10.1007/BF00225876.
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.
研究了口服氯化钙溶液的大鼠脑内钙蓄积的特征。大鼠单次口服钙（15 - 50毫克/100克体重），并在给药后15至120分钟之间通过放血处死。给予钙（50毫克/100克）导致血清钙浓度显著升高以及脑钙含量相应升高，表明钙向脑内的转运与血清钙水平的升高有关。预先用Ca2+通道阻滞剂（维拉帕米或地尔硫䓬，剂量为1.5和3.0毫克/100克）处理，钙给药引起的脑钙含量增加没有明显改变。在甲状旁腺切除的大鼠中，给予钙（50毫克/100克）导致脑钙含量显著增加，表明钙调节激素不参与脑钙转运。现在，禁食（过夜）明显提高了脑钙含量，尽管血清钙水平没有显著改变。与对照（禁食）大鼠相比，给禁食大鼠补钙导致脑钙含量进一步升高。禁食引起的脑钙含量增加通过重新喂食明显恢复。给禁食大鼠口服葡萄糖（0.4克/100克）也能看到这种恢复。本研究表明血清钙被转运到脑内，并且增加的脑钙会迅速释放。脑内钙的释放可能参与能量代谢，并且这种释放可能因脑内葡萄糖供应减少而减弱。这一发现表明能量依赖机制在脑钙调节中的生理意义。
