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SALIVARY GLAND SECRETORY MECHANISMS DURING NORMAL AND ALTERED FUNCTIONAL STATES

SALIVARY GLAND SECRETORY MECHANISMS DURING NORMAL AND ALTERED FUNCTIONAL STATES
正常和功能改变状态下的唾液腺分泌机制
批准号:
3839193
负责人:
B J BAUM
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
口腔的健康是由唾液分泌物维持的。 公关 UNR 唾液腺的功能是产生这些复杂的液体。 我们利用 离体 分散的唾液腺细胞,以了解控制唾液腺的机制, 一个编队。 我们的研究主要集中在神经递质对分泌期细胞的调节上, s和 相关的信号机制。 在本报告所述期间, 研究领域 在大鼠腮腺腺泡细胞中, ls及其 通过特定的G蛋白偶联到功能反应。 我们也有ini 过时的研究 肾上腺素能受体(alpha 1-ARs)的表达。 腮腺细胞 刺激 mAChRs的激活导致肌醇磷酸的产生, 的 磷脂酰肌醇4,5-二磷酸特异性磷脂酶C。 后续 这 反应导致细胞内Ca 2+水平升高和体液分泌增加, 此外,mAChR可介导激动剂诱导的cAMP的抑制, 是的。 我们 已经表征了亚型非选择性拮抗剂(quinu 烷基 二苯甲酸酯,QNB)与完整大鼠腮腺细胞中的mAChR。 特异性结合 可饱和的, 时间和温度依赖性(Bmax约80 fmol/mg蛋白; Kd 近似 100 pM)。 此外,我们还评估了mAChR占用率与 二 信使的形成,决定了适度的人口(大约 -40%) 存在用于三磷酸肌醇(IP 3)形成备用受体。 我们的团队 sly报道 大鼠腮腺M3-mAChR与两种不同信号转导G蛋白偶联 ins. 这 2004年,我们确定了编码该区域的核苷酸序列, 或基因 参与G蛋白偶联,我们观察到它实际上是 到其他 报道了3个序列。 因此,mAChR本身不太可能负责。 为 发散耦合 此外,我们已经表明,α 1-肾上腺素能 受体 参与液体分泌反应的亚型是α 1A。
英文摘要
The health of the oral cavity is maintained by salivary secretions. The pr cipal function of salivary glands is to produce these complex fluids. We utilize n vitro dispersed cells of salivary glands to understand mechanisms controlling sal a formation. We have focused our studies on neurotransmitter regulation of secretory eve s and associated signalling mechanisms. During this reporting period the primary ocus of study continues to be muscarinic receptors (mAChRs) in rat parotid gland acinar c ls and their coupling to functional responses via specific G proteins. We have also ini ated studies of alpha-adrenergic receptors (alpha1-ARs) in these cells. In parotid cell stimulation of mAChRs results in the generation of inositol phosphates via the activati of a phosphatidylinositol 4,5-bisphosphate specific phospholipase C. Subsequent this response leads to the elevation of cytosolic Ca2+ levels and fluid secretio Additionally, mAChRs can mediate the inhibition of agonist induced cAMP for tion. We have characterized the binding of a subtype non-selective antagonist (quinu idinyl benzilate, QNB) to mAChRs in intact rat parotid cells. Specific binding is aturable, time- and temperature-dependent (Bmax approximately 80 fmol/mg protein; Kd proximately 100 pM). Also, we have assessed the relationship between mAChR occupancy a second messenger formation, determining that a moderate population (approximately -40%) of spare receptors exist for inositol trisphosphate (IP3) formation. We previ sly reported that rat parotid M3-mAChRs couple to two different signal transducing G pro ins. This year we determined the nucleotide sequence encoding the region of this rece or gene involved in G-protein coupling and we observed that it is virtually identic to other reported 3 sequences. Thus, the mAChR itself is unlikely to be responsibl for the divergent coupling. Additionally, we have shown that the alpha1-adrenergic eceptor subtype involved in the fluid secretory response is alpha1A.
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SALIVARY GLAND SECRETORY MECHANISMS DURING NORMAL AND ALTERED FUNCTIONAL STATES
SALIVARY GLAND SECRETORY MECHANISMS DURING NORMAL AND ALTERED FUNCTIONAL STATES
SALIVARY GLAND SECRETORY MECHANISMS DURING NORMAL AND ALTERED FUNCTIONAL STATES
SALIVARY GLAND SECRETORY MECHANISMS DURING NORMAL AND ALTERED FUNCTIONAL STATES
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