Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction
Interactions between adenosine and phorbol esters or lithium at the frog neuromuscular junction
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腺苷和佛波酯或锂在青蛙神经肌肉接头处的相互作用
DOI：
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发表时间：
1990
影响因子：
7.3
通讯作者：
J. Ribeiro
中科院分区：
文献类型：
--
作者：
A. Sebastião;J. Ribeiro
1研究了腺苷或2-氯腺苷（CADO）的作用与干扰磷酸肌醇/蛋白激酶C转导系统或腺苷酸环化酶转导系统的物质对终板电位的作用之间的相互作用（e.p.ps）。所用的制剂是神经支配的缝匠肌的青蛙，其中抽搐已被阻止与高镁浓度。2蛋白激酶C激活剂4β-佛波醇-12，13-二乙酸酯（PDAc）可逆性地增加e.p.ps的振幅和量子含量，减弱腺苷和CADO对e. p. p.振幅的抑制作用。腺苷受体拮抗剂8-苯基茶碱的亲和力未被PDAc改变。3不激活蛋白激酶C的佛波酯4α-佛波醇-12，13-二癸酸酯既不改变e. p. p.振幅，也不改变腺苷对e. p. p.的抑制作用。4蛋白激酶C抑制剂多粘菌素B可逆性地降低E. p. e.p.ps幅值和量子含量，阻止PDAc引起的E. p. p.幅值的增加，但不改变腺苷对E. p. p.的抑制作用。另一种蛋白激酶抑制剂H-7也降低了e. p. p.振幅，但没有改变PDAc对e. p. p.振幅的影响。5氯化锂通过抑制肌醇磷酸的分解而改变磷酸肌醇信号转导，可逆地增加了e.p.ps的振幅和量子含量。在腺苷或CADO存在下，锂对e. p. p.振幅的影响显著减弱。6腺苷酸环化酶激活剂forskolin可逆性地增加诱发电位的幅度和量子含量。MDL 12，330 A是腺苷酸环化酶的抑制剂，可不可逆地降低e. p. p.振幅，这种作用可被毛喉素阻止。毛喉素和MDL 12，330 A均不改变腺苷对e.p.ps的抑制作用。结果提示，腺苷对神经肌肉传递的抑制作用可能与磷酸肌醇/蛋白激酶C转导系统有关，而与腺苷酸环化酶转导系统无关。
1 Interactions between the effects of adenosine or 2‐chloro‐adenosine (CADO) and the effects of substances that interfere with the phosphoinositides/protein kinase C transducing system or with the adenylate cyclase transducing system, on endplate potentials (e.p.ps), were investigated. The preparation used was the innervated sartorius muscle of the frog in which twitches had been prevented with high magnesium concentrations. 2 The activator of protein kinase C, 4β‐phorbol‐12,13‐diacetate (PDAc), reversibly increased the amplitude and the quantal content of e.p.ps and attenuated the inhibitory effects of adenosine and CADO on e.p.p. amplitude. The affinity of the adenosine receptor antagonist, 8‐phenyltheophylline, was not modified by PDAc. 3 The phorbol ester 4α‐phorbol‐12,13‐didecanoate, which does not activate protein kinase C, did not modify either e.p.p. amplitude or the inhibitory effect of adenosine on e.p.ps. 4 The inhibitor of protein kinase C, polymyxin B, reversibly decreased the amplitude and the quantal content of e.p.ps, prevented the enhancement caused by PDAc on e.p.p. amplitude, but did not modify the inhibitory effect of adenosine on e.p.ps. H‐7, another inhibitor of protein kinases, also decreased e.p.p. amplitude but did not modify the effect of PDAc on the amplitude of e.p.ps. 5 Lithium chloride, which alters phosphoinositide signal transduction by inhibiting the breakdown of inositol phosphates, reversibly increased the amplitude and the quantal content of the e.p.ps. In the presence of adenosine or CADO the effect of lithium on e.p.p. amplitude was markedly attenuated. 6 The activator of adenylate cyclase, forskolin, reversibly increased the amplitude and the quantal content of the e.p.ps. MDL 12,330A, an inhibitor of adenylate cyclase, irreversibly decreased e.p.p. amplitude, an effect which was prevented by forskolin. Neither forskolin nor MDL 12,330A modified the inhibitory effect of adenosine on e.p.ps. 7 The results suggest that the phosphoinositides/protein kinase C transducing system, but not the adenylate cyclase transducing system, might be involved in the inhibitory effect of adenosine on neuromuscular transmission.
通过腺苷 A1 受体调节 GH3 细胞功能。
DOI：
10.1042/bj2550069
发表时间：
1988
期刊：
The Biochemical journal
影响因子：
--
作者：
Delahunty,TM;Cronin,MJ;Linden,J
通讯作者：
Linden,J
钙动员受体、多磷酸肌醇和第二信使的产生。
影响因子：
21.1
作者：
Abdel-Latif,AA
通讯作者：
Abdel-Latif,AA
腺苷受体激动剂抑制大鼠纹状体切片中磷酸肌醇的积累。
影响因子：
5
作者：
Petcoff,DW;Cooper,DM
通讯作者：
Cooper,DM