| First Author | Pang ZP | Year | 2011 |
| Journal | Neuron | Volume | 70 |
| Issue | 2 | Pages | 244-51 |
| PubMed ID | 21521611 | Mgi Jnum | J:174823 |
| Mgi Id | MGI:5141208 | Doi | 10.1016/j.neuron.2011.03.011 |
| Citation | Pang ZP, et al. (2011) Doc2 supports spontaneous synaptic transmission by a Ca(2+)-independent mechanism. Neuron 70(2):244-51 |
| abstractText | Two families of Ca(2+)-binding proteins have been proposed as Ca(2+) sensors for spontaneous release: synaptotagmins and Doc2s, with the intriguing possibility that Doc2s may represent high-affinity Ca(2+) sensors that are activated by deletion of synaptotagmins, thereby accounting for the increased spontaneous release in synaptotagmin-deficient synapses. Here, we use an shRNA-dependent quadruple knockdown of all four Ca(2+)-binding proteins of the Doc2 family to confirm that Doc2-deficient synapses exhibit a marked decrease in the frequency of spontaneous release events. Knockdown of Doc2s in synaptotagmin-1-deficient synapses, however, failed to reduce either the increased spontaneous release or the decreased evoked release of these synapses, suggesting that Doc2s do not constitute Ca(2+) sensors for asynchronous release. Moreover, rescue experiments revealed that the decrease in spontaneous release induced by the Doc2 knockdown in wild-type synapses is fully reversed by mutant Doc2B lacking Ca(2+)-binding sites. Thus, our data suggest that Doc2s are modulators of spontaneous synaptic transmission that act by a Ca(2+)-independent mechanism. |
