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首页> 外文期刊>Journal of Neurophysiology >Sweet taste transduction in hamster: role of protein kinases.
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Sweet taste transduction in hamster: role of protein kinases.

机译：仓鼠的甜味转导：蛋白激酶的作用。

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Two different second-messenger pathways have been implicated in sweet taste transduction: sugars produce cyclic AMP (cAMP), whereas synthetic sweeteners stimulate production of inositol 1,4, 5-tris-phosphate (IP(3)) and diacylglycerol (DAG). Both sugars and sweeteners depolarize taste cells by blocking the same resting K(+) conductance, but the intermediate steps in the transduction pathways have not been examined. In this study, the loose-patch recording technique was used to examine the role of protein kinases and other downstream regulatory proteins in the two sweet transduction pathways. Bursts of action currents were elicited from approximately 35% of fungiform taste buds in response to sucrose (200 mM) or NC-00274-01 (NC-01, 200 microM), a synthetic sweetener. To determine whether protein kinase C (PKC) plays a role in sweet transduction, taste buds were stimulated with the PKC activator PDBu (10 microM). In all sweet-responsive taste buds tested (n = 11), PDBu elicited burst of action currents. In contrast, PDBu elicited responses in only 4 of 19 sweet-unresponsive taste buds. Inhibition of PKC by bisindolylmaleimide I (0.15 microM) resulted in inhibition of the NC-01 response by approximately 75%, whereas the response to sucrose either increased or remained unchanged. These data suggest that activation of PKC is required for the transduction of synthetic sweeteners. To determine whether protein kinase A (PKA) is required for the transduction of sugars, sweet responses were examined in the presence of the membrane-permeant PKA inhibitor H-89 (10 and 19 microM). Surprisingly, H-89 did not decrease responses to either sucrose or NC-01. Instead, responses to both compounds were increased in the presence of the inhibitor. These data suggest that PKA is not required for the transduction of sugars, but may play a modulatory role in both pathways, such as adaptation of the response. We also examined whether Ca(2+)-calmodulin dependent cAMP phosphodiesterase (CaM-PDE) plays a role in sweet taste transduction, by examining responses to sucrose and synthetic sweeteners in the presence of the CaM-PDE inhibitor W-7 (100 microM). Inhibition resulted in an increase in the response to sucrose, whereas the response to NC-01 remained unchanged. These data suggest that the pathways for sugars and sweeteners are negatively coupled; the Ca(2+) that is released from intracellular stores during stimulation with synthetic sweeteners may inhibit the response to sucrose by activation of CaM-PDE.
机译：甜味转导涉及两个不同的第二信使途径：糖产生环状AMP（cAMP），而合成甜味剂刺激肌醇1,4、5-三磷酸（IP（3））和二酰基甘油（DAG）的产生。糖和甜味剂都通过阻断相同的静止K（+）电导来使味觉细胞去极化，但是转导途径的中间步骤尚未得到检验。在这项研究中，使用松弛补丁记录技术来检查蛋白激酶和其他下游调节蛋白在这两个甜味转导途径中的作用。响应蔗糖（200 mM）或合成甜味剂NC-00274-01（NC-01，200 microM），大约35％的真菌状味蕾引发了作用电流的爆发。为了确定蛋白激酶C（PKC）是否在甜味转导中起作用，用PKC激活剂PDBu（10 microM）刺激了味蕾。在所有测试的对甜味敏感的味蕾中（n = 11），PDBu引起了动作电流爆发。相反，PDBu仅在19个无甜味的味蕾中引起4个响应。双辛基马来酰亚胺I（0.15 microM）对PKC的抑制作用导致对NC-01反应的抑制作用约为75％，而对蔗糖的反应则增加或保持不变。这些数据表明，PKC的活化是合成甜味剂转导所必需的。为了确定糖激酶的转导是否需要蛋白激酶A（PKA），在存在可透过膜的PKA抑制剂H-89（10和19 microM）的情况下检查了甜味反应。出乎意料的是，H-89并未降低对蔗糖或NC-01的反应。相反，在抑制剂存在下，对两种化合物的反应都增加了。这些数据表明，糖的转导不需要PKA，但是PKA可能在两种途径中都起调节作用，例如响应的适应。我们还检查了Ca（2 +）-钙调蛋白依赖性cAMP磷酸二酯酶（CaM-PDE）是否在甜味传递中发挥作用，方法是在CaM-PDE抑制剂W-7（100 microM）存在下检查对蔗糖和合成甜味剂的反应）。抑制作用导致对蔗糖的反应增加，而对NC-01的反应保持不变。这些数据表明糖和甜味剂的途径是负相关的。合成甜味剂刺激过程中从细胞内存储释放的Ca（2+）可能会通过激活CaM-PDE来抑制对蔗糖的反应。

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