The transient receptor potential (TrpA—ankyrin) receptor has been linked to pathological conditions in cardiac function in mammals. To better understand the function of the TrpA1 in regulation of the heart, a Drosophila melanogaster model was used to express TrpA1 in heart and body wall muscles. Heartbeat of in intact larvae as well as hearts in situ, devoid of hormonal and neural input, indicate that strong over-expression of TrpA1 in larvae at 30 or 37 °C stopped the heart from beating, but in a diastolic state. Cardiac function recovered upon cooling after short exposure to high temperature. Parental control larvae (UAS-TrpA1) increased heart rate transiently at 30 and 37 °C but slowed at 37 °C within 3 min for in-situ preparations, while in-vivo larvae maintained a constant heart rate. The in-situ preparations maintained an elevated rate at 30 °C. The heartbeat in the TrpA1-expressing strains could not be revived at 37 °C with serotonin. Thus, TrpA1 activation may have allowed enough Ca²⁺ influx to activate K(_Ca) channels into a form of diastolic stasis. TrpA1 activation in body wall muscle confirmed a depolarization of membrane. In contrast, blowfly Phaenicia sericata larvae increased heartbeat at 30 and 37 °C, demonstrating greater cardiac thermotolerance.

中文翻译：

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温度对 TrpA1 受体表达改变的丝光雉鸡和黑腹果蝇心率的影响


瞬时受体电位（TrpA-锚蛋白）受体与哺乳动物心脏功能的病理状况有关。为了更好地了解 TrpA1 在心脏调节中的功能，使用果蝇模型在心脏和体壁肌肉中表达 TrpA1。完整幼虫以及原位心脏（缺乏激素和神经输入）的心跳表明，在 30 或 37°C 时，幼虫中 TrpA1 的强烈过度表达使心脏停止跳动，但处于舒张状态。短暂暴露于高温后冷却后心脏功能恢复。亲代对照幼虫 (UAS-TrpA1) 在 30 和 37 °C 下心率短暂增加，但在 37 °C 下原位制备 3 分钟内心率减慢，而体内幼虫则保持恒定心率。原位制备在 30°C 下保持较高的速率。表达 TrpA1 的菌株的心跳在 37°C 时无法用血清素恢复。因此，TrpA1 激活可能允许足够的 Ca ²⁺流入，以激活 K( _Ca ) 通道进入舒张期停滞形式。体壁肌肉中 TrpA1 的激活证实了膜的去极化。相比之下，绿头苍蝇幼虫在 30 和 37 °C 时心跳加快，表现出更强的心脏耐热性。