| First Author | Schlüter OM | Year | 2006 |
| Journal | J Neurosci | Volume | 26 |
| Issue | 4 | Pages | 1239-46 |
| PubMed ID | 16436611 | Mgi Jnum | J:104983 |
| Mgi Id | MGI:3613252 | Doi | 10.1523/JNEUROSCI.3553-05.2006 |
| Citation | Schluter OM, et al. (2006) Rab3 superprimes synaptic vesicles for release: implications for short-term synaptic plasticity. J Neurosci 26(4):1239-46 |
| abstractText | Presynaptic vesicle trafficking and priming are important steps in regulating synaptic transmission and plasticity. The four closely related small GTP-binding proteins Rab3A, Rab3B, Rab3C, and Rab3D are believed to be important for these steps. In mice, the complete absence of all Rab3s leads to perinatal lethality accompanied by a 30% reduction of probability of Ca2+-triggered synaptic release. This study examines the role of Rab3 during Ca2+-triggered release in more detail and identifies its impact on short-term plasticity. Using patch-clamp electrophysiology of autaptic neuronal cultures from Rab3-deficient mouse hippocampus, we show that excitatory Rab3-deficient neurons display unique time- and frequency-dependent short-term plasticity characteristics in response to spike trains. Analysis of vesicle release and repriming kinetics as well as Ca2+ sensitivity of release indicate that Rab3 acts on a subset of primed, fusion competent vesicles. They lower the amount of Ca2+ required for action potential-triggered release, which leads to a boosting of release probability, but their action also introduces a significant delay in the supply of these modified vesicles. As a result, Rab3-induced modifications to primed vesicles causes a transient increase in the transduction efficacy of synaptic action potential trains and optimizes the encoding of synaptic information at an intermediate spike frequency range. |
