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首页> 外文期刊>The Journal of Physiology >G protein {beta}{gamma} subunits mediate presynaptic inhibition of transmitter release from rat superior cervical ganglion neurones in culture.
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G protein {beta}{gamma} subunits mediate presynaptic inhibition of transmitter release from rat superior cervical ganglion neurones in culture.

机译：G蛋白{beta} {γ}亚基介导突触前抑制培养物中大鼠上颈神经节神经元释放递质。

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The activation of presynaptic G protein-coupled receptors (GPCRs) is widely reported to inhibit transmitter release; however, the lack of accessibility of many presynaptic terminals has limited direct analysis of signalling mediators. We studied GPCR-mediated inhibition of fast cholinergic transmission between superior cervical ganglion neurones (SCGNs) in culture. The adrenoceptor agonist noradrenaline (NA) caused a dose-related reduction in evoked excitatory postsynaptic potentials (EPSPs). NA-induced EPSP decrease was accompanied by effects on the presynaptic action potential (AP), reducing AP duration and amplitude of the after-hyperpolarization (AHP), without affecting the pre- and postsynaptic membrane potential. All effects of NA were blocked by yohimbine and synaptic transmission was reduced by clonidine, consistent with an action at presynaptic alpha2-adrenoceptors. NA-induced inhibition of transmission was sensitive to pre-incubation of SCGNs with pertussis toxin (PTX), implicating the involvement of Galpha(i/o)betagamma subunits. Expression of Galpha transducin, an agent which sequesters G protein betagamma (Gbetagamma) subunits, in the presynaptic neurone caused a time-dependent attenuation of NA-induced inhibition. Injection of purified Gbetagamma subunits into the presynaptic neurone inhibited transmission, and also reduced the AHP amplitude. Furthermore, NA-induced inhibition was occluded by pre-injection of Gbetagamma subunits. The Ca(2+) channel blocker Cd(2+) mimicked NA effects on transmitter release. Cd(2+), NA and Gbetagamma subunits also inhibited somatic Ca(2+) current. In contrast to effects on AP-evoked transmitter release, NA had no clear action on AP-independent EPSPs induced by hypertonic solutions. These results demonstrate that Gbetagamma subunits functionally mediate inhibition of transmitter release by alpha2-adrenoceptors and represent important regulators of synaptic transmission at mammalian presynaptic terminals.
机译：广泛报道了突触前G蛋白偶联受体（GPCR）的激活抑制了递质的释放。然而，许多突触前末端的可及性的缺乏限制了信号介体的直接分析。我们研究了GPCR介导的上层颈神经节神经元（SCGNs）之间快速胆碱能传递的抑制。肾上腺素受体激动剂去甲肾上腺素（NA）引起与剂量相关的诱发兴奋性突触后电位（EPSPs）降低。 NA诱导的EPSP降低伴随着对突触前动作电位（AP）的影响，减少AP持续时间和超极化后（AHP）的幅度，而不影响突触前和突触后膜电位。育亨宾可阻断NA的所有作用，可乐定可降低突触传递，这与对突触前α2-肾上腺素受体的作用一致。 NA诱导的传播抑制对SCGNs与百日咳毒素（PTX）的预培养很敏感，这牵涉到Galpha（i / o）betagamma亚基的参与。在突触前神经元中，Galpha转导蛋白（一种隔离G蛋白betagamma（Gbetagamma）亚基的试剂）的表达引起了NA诱导的抑制作用的时间依赖性衰减。纯化的Gbetagamma亚基注射到突触前神经元抑制传播，也降低了AHP振幅。此外，通过预先注射Gbetagamma亚基可阻断NA诱导的抑制作用。 Ca（2+）通道阻滞剂Cd（2+）模仿NA对发射器释放的影响。 Cd（2+），NA和Gbetagamma亚基也抑制体细胞Ca（2+）电流。与对AP诱发的发射器释放的影响相反，NA对高渗溶液诱导的非AP依赖性EPSP没有明显作用。这些结果表明，Gbetagamma亚基功能上介导α2-肾上腺素受体对递质释放的抑制，并且代表了哺乳动物突触前末端突触传递的重要调节剂。

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