科研之友
微信
新浪微博
Facebook
分享链接
摘要
G-protein beta gamma subunits (G beta gamma) interact with presynaptic proteins and regulate neurotransmitter release downstream of Ca2+ influx. To accomplish their roles in sensory signaling, photoreceptor synapses use specialized presynaptic proteins that support neurotransmission at active zone structures known as ribbons. While several G-protein coupled receptors (GPCRs) influence synaptic transmission at ribbon synapses of cones and other retinal neurons, it is unknown whether G beta gamma contributes to these effects. We tested whether activation of one particular GPCR, a metabotropic glutamate receptor (mGluR), can reduce cone synaptic transmission via G beta gamma in tiger salamander retinas. In recordings from horizontal cells, we found that an mGluR agonist (L-AP4) reduced cone-driven light responses and mEPSC frequency. In paired recordings of cones and horizontal cells, L-AP4 slightly reduced cone I-Ca (similar to 10%) and caused a larger reduction in cone-driven EPSCs (similar to 30%). Proximity ligation assay revealed direct interactions between SNAP-25 and G beta gamma subunits in retinal synaptic layers. Pretreatment with the SNAP-25 cleaving protease BoNT/A inhibited L-AP4 effects on synaptic transmission, as did introduction of a peptide derived from the SNAP-25 Cterminus. Introducing G beta gamma subunits directly into cones reduced EPSC amplitude. This effect was inhibited by BoNT/A, supporting a role for G beta gamma/SNAP-25 interactions. However, the mGluR-dependent reduction in I-Ca was not mimicked by G beta gamma, indicating that this effect was independent of G beta gamma. The finding that synaptic transmission at cone ribbon synapses is regulated by G beta gamma/SNAP-25 interactions indicates that these mechanisms are shared by conventional and ribbon-type synapses. G beta gamma liberated from other photoreceptor GPCRs is also likely to regulate synaptic transmission.
- 出版日期2017-4-26
