| First Author | Dudanova I | Year | 2006 |
| Journal | J Neurosci | Volume | 26 |
| Issue | 41 | Pages | 10599-613 |
| PubMed ID | 17035546 | Mgi Jnum | J:113228 |
| Mgi Id | MGI:3664827 | Doi | 10.1523/JNEUROSCI.1913-06.2006 |
| Citation | Dudanova I, et al. (2006) Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules. J Neurosci 26(41):10599-613 |
| abstractText | Alpha-neurexins constitute a family of neuronal cell surface molecules that are essential for efficient neurotransmission, because mice lacking two or all three alpha-neurexin genes show a severe reduction of synaptic release. Although analyses of alpha-neurexin knock-outs and transgenic rescue animals suggested an involvement of voltage-dependent Ca2+ channels, it remained unclear whether alpha-neurexins have a general role in Ca2+-dependent exocytosis and how they may affect Ca2+ channels. Here we show by membrane capacitance measurements from melanotrophs in acute pituitary gland slices that release from endocrine cells is diminished by >50% in adult alpha-neurexin double knock-out and newborn triple knock-out mice. There is a reduction of the cell volume in mutant melanotrophs; however, no ultrastructural changes in size or intracellular distribution of the secretory granules were observed. Recordings of Ca2+ currents from melanotrophs, transfected human embryonic kidney cells, and brainstem neurons reveal that alpha-neurexins do not affect the activation or inactivation properties of Ca2+ channels directly but may be responsible for coupling them to release-ready vesicles and metabotropic receptors. Our data support a general and essential role for alpha-neurexins in Ca2+-triggered exocytosis that is similarly important for secretion from neurons and endocrine cells. |
