| First Author | Walaas SI | Year | 2000 |
| Journal | Synapse | Volume | 36 |
| Issue | 2 | Pages | 114-9 |
| PubMed ID | 10767058 | Mgi Jnum | J:62366 |
| Mgi Id | MGI:1858805 | Doi | 10.1002/(SICI)1098-2396(200005)36:2<114::AID-SYN4>3.0.CO;2-Q |
| Citation | Walaas SI, et al. (2000) Decrease in phorbol ester-induced potentiation of noradrenaline release in synapsin I-deficient mice. Synapse 36(2):114-9 |
| abstractText | Synapsin I is involved in regulating amino acid neurotransmitter release, but has a less clear role in noradrenergic nerve terminals. To better understand the role of synapsin I in the function of noradrenergic nerve terminals, we compared noradrenaline release in wild-type and synapsin I-deficient mice. No difference was found in the accumulation or in the Ca(2+)-independent release of [(3)H]noradrenaline in cerebrocortical synaptosomes from wild-type and synapsin I-deficient mice. Synaptosomes lacking synapsin I also displayed no gross alterations in either the time course or the Ca(2+)-dependency of [(3)H]noradrenaline release when stimulated by depolarizing secretagogues or ionophore treatment. In wild-type synaptosomes, activation of protein kinase C by phorbol ester treatment resulted in a Ca(2+)-dependent increase in [(3)H]noradrenaline release evoked by depolarizing secretagogues and ionophore treatment. The phorbol ester-mediated enhancement of [(3)H]noradrenaline release evoked by depolarizing secretagogues, but not by ionophore treatment, was greatly reduced in synapsin I-deficient synaptosomes. These results indicate that synapsin I plays a role in regulating noradrenaline release. Copyright 2000 Wiley-Liss, Inc. |
