An increase in intracelluar free calcium ions modulated by cholinergic receptors in rat facial nucleus  

作　　者：SUN Da-wei ZHOU Rui LI Na ZHANG Qiu-gui ZHU Fu-gao 

机构地区：[1]Department of Otolaryngology, Affiliated Hospital of MedicalCollege, Qingdao University, Qingdao, Shandong 266003, China [2]Qingdao Hiser Medical Center, Qingdao, Shandong 266033, China

出　　处：《Chinese Medical Journal》2009年第9期1049-1055,共7页中华医学杂志（英文版）

基　　金：This work was supported by a grant from the Youth Science Foundation of Qingdao University （No. 2007）.

摘　　要：Background Ca^2＋ in the central nervous system plays important roles in brain physiology, including neuronal survival and regeneration in rats with injured facial motoneurons. The present research was to study the modulations of intracellular free Ca^2＋ concentrations by cholinergic receptors in rat facial nucleus, and the mechanisms of the modulations. Methods The fluorescence intensity of facial nucleus in Fluo-3 AM loaded acute brainstem slices was detected by applying intracellular free Ca^2＋ measurement technique via confocal laser scanning microscope. The changes of fluorescence intensity of facial nucleus indicate the average changes of intracellular free Ca^2＋ levels of the neurons. Results Acetylcholine was effective at increasing the fluorescence intensity of facial nucleus. Muscarine chloride induced a marked increase of fluorescence intensity in a concentration dependent fashion. The enhancement of fluorescence intensity by muscarine chloride was significantly reduced by thapsigargin （depletor of intracellular Ca^2＋ store; P 〈0.01）, rather than Ca^2＋ free artifical cerebrospinal fluid or EGTA （free Ca^2＋ chelator; P〉0.05）. And the increase of fluorescence intensity was also significantly inhibited by pirenzepine （M1 subtype selective antagonist; P 〈0.01） and 4-DAMP （M3 subtype selective antagonist; P 〈0.01）. In addition, fluorescence intensity was markedly increased by nicotine. The enhancement of fluorescence intensity by nicotine was significantly reduced by EGTA, nifedipine （L-type voltage-gated Ca^2＋ channel blocker）, dihydro-β-erythroidine （α4β2 subtype selective antagonist）, and in Ca^2＋ free artificial cerebrospinal fluid （P 〈0.01）, but not in the presence of mibefradil （M-type voltage-gated Ca^2＋ channel blocker） or thapsigargin （P〉0.05）. Conclusions The data provide the evidence that muscarinic receptors may induce the increase of intracellular free Ca^2＋ levels through the Ca^2＋ release of intracellular Ca^2＋ storesBackground Ca^2＋ in the central nervous system plays important roles in brain physiology, including neuronal survival and regeneration in rats with injured facial motoneurons. The present research was to study the modulations of intracellular free Ca^2＋ concentrations by cholinergic receptors in rat facial nucleus, and the mechanisms of the modulations. Methods The fluorescence intensity of facial nucleus in Fluo-3 AM loaded acute brainstem slices was detected by applying intracellular free Ca^2＋ measurement technique via confocal laser scanning microscope. The changes of fluorescence intensity of facial nucleus indicate the average changes of intracellular free Ca^2＋ levels of the neurons. Results Acetylcholine was effective at increasing the fluorescence intensity of facial nucleus. Muscarine chloride induced a marked increase of fluorescence intensity in a concentration dependent fashion. The enhancement of fluorescence intensity by muscarine chloride was significantly reduced by thapsigargin （depletor of intracellular Ca^2＋ store; P 〈0.01）, rather than Ca^2＋ free artifical cerebrospinal fluid or EGTA （free Ca^2＋ chelator; P〉0.05）. And the increase of fluorescence intensity was also significantly inhibited by pirenzepine （M1 subtype selective antagonist; P 〈0.01） and 4-DAMP （M3 subtype selective antagonist; P 〈0.01）. In addition, fluorescence intensity was markedly increased by nicotine. The enhancement of fluorescence intensity by nicotine was significantly reduced by EGTA, nifedipine （L-type voltage-gated Ca^2＋ channel blocker）, dihydro-β-erythroidine （α4β2 subtype selective antagonist）, and in Ca^2＋ free artificial cerebrospinal fluid （P 〈0.01）, but not in the presence of mibefradil （M-type voltage-gated Ca^2＋ channel blocker） or thapsigargin （P〉0.05）. Conclusions The data provide the evidence that muscarinic receptors may induce the increase of intracellular free Ca^2＋ levels through the Ca^2＋ release of intracellular Ca^2＋ stores

关 键 词：calcium signaling receptors  cholinergic facial nerve 

分 类 号：R735.35[医药卫生—肿瘤] R651.3[医药卫生—临床医学]