Signaling pathway underlying the octopaminergic modulation of myogenic contraction in the cricket lateral oviduct.
Signaling pathway underlying the octopaminergic modulation of myogenic contraction in the cricket lateral oviduct.
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DOI：
10.1016/j.jinsphys.2014.09.010
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发表时间：
2014-12
影响因子：
2.2
通讯作者：
Hirotake Tamashiro;M. Yoshino
中科院分区：
文献类型：
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作者：
Hirotake Tamashiro;M. Yoshino
章鱼胺（Octopamine，OA）是一种生物源性单胺，在无脊椎动物中是一种神经递质和神经调质。本文报道了OA对蟋蟀（Gryllus bimaculatus）输卵管外侧壁自发节律性收缩（SRCs）的影响及其可能的信号通路。应用OA以剂量依赖性方式增加SRCs的频率和振幅。随后应用OA受体拮抗剂依匹斯汀可抑制OA的作用，表明OA的作用由OA受体介导。为了研究OA作用的主要信号通路，我们首先研究了cAMP/cAMP依赖性蛋白激酶A（PKA）信号通路的可能参与。应用膜渗透性cAMP类似物8-Br-cAMP对SRCs的影响很小，OA的作用不受随后应用PKA抑制剂H89的影响，表明cAMP/PKA信号通路不是OA作用的主要通路。接下来，我们研究了第二信使肌醇1，4，5-三磷酸在OA作用中的可能参与。OA对SRCs的影响被随后应用的磷脂酰肌醇特异性磷脂酶C（PLC）抑制剂U 73122抑制，表明PLC途径参与OA的作用。用ryanodine受体拮抗剂丁卡因预处理细胞可抑制OA诱导的SRCs频率增加，但IP 3受体拮抗剂2-氨基乙氧基二苯基硼酸酯（2-APB）对OA诱导的SRCs频率增加无明显影响。另一方面，OA诱导的SRCs振幅的增加被2-APB预处理的细胞抑制，但丁卡因没有显着影响。这些结果提示，OA对SRCs的兴奋作用是通过PLC信号通路介导的：IP 3受体的Ca 2+释放可能参与SRCs振幅的调节，而ryanodine受体的Ca 2+释放可能参与SRCs频率的调节。
Octopamine (OA), a biogenic monoamine, is a neurotransmitter and neuromodulator in invertebrates. Here, we report the effect of OA on the spontaneous rhythmic contractions (SRCs) of the lateral oviduct of the cricketGryllus bimaculatusand the possible signaling pathway involved. Application of OA increased both the frequency and amplitude of SRCs in a dose-dependent manner. The effect of OA was inhibited by subsequent application of the OA receptor antagonist epinastine, indicating that the action of OA is mediated by OA receptor. To investigate the predominant signaling pathway underlying the action of OA, we first examined a possible involvement of the cAMP/cAMP-dependent protein kinase A (PKA) signaling pathway. Application of the membrane-permeable cAMP analog 8-Br-cAMP had little effect on SRCs and the effect of OA was not influenced by subsequent application of the PKA inhibitor H89, indicating that the cAMP/PKA signaling pathway is not the predominant pathway in the action of OA. Next, we examined a possible involvement of the second messenger inositol 1,4,5-trisphosphate in the action of OA. The effect of OA on SRCs was inhibited by subsequent application of the phosphoinositide-specific phospholipase C (PLC) inhibitor U73122, indicating that the PLC pathway is involved in the action of OA. The OA-induced increase in the frequency of SRCs was inhibited by pretreatment of the cell with the ryanodine receptor antagonist tetracaine but was not significantly affected by the IP3receptor antagonist 2-aminoethoxydiphenyl borate (2-APB). On the other hand, the OA-induced increase in the amplitude of SRCs was inhibited by pretreatment of the cells with 2-APB but was not significantly affected by tetracaine. Taken together, these results suggest that the OA-induced excitatory effect on SRCs is mediated by the PLC signaling pathway: Ca2+release from IP3receptors may contribute to the modulation of the amplitude of SRCs, whereas Ca2+release from ryanodine receptors may contribute to the modulation of the frequency of SRCs.