ACETYLCHOLINE EXOCYTOSIS IN PC12 CELLS DEFICIENT IN SNAP-25

Citation
P. Ray et al., ACETYLCHOLINE EXOCYTOSIS IN PC12 CELLS DEFICIENT IN SNAP-25, NeuroReport, 8(9-10), 1997, pp. 2271-2274
Citations number
24
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
09594965
Volume
8
Issue
9-10
Year of publication
1997
Pages
2271 - 2274
Database
ISI
SICI code
0959-4965(1997)8:9-10<2271:AEIPCD>2.0.ZU;2-Q
Abstract
STIMULUS-INDUCED acetylcholine (ACh) exocytosis from presynaptic nerve terminals involves two important steps: fusion of ACh loaded vesicles at presynaptic release sites, followed by release into the synaptic c left. We studied the role of the putative vesicle fusion protein SNAP- 25 in this process. The nerve growth factor-differentiated PC12 cell l ine was used as an experimental model. A bee venom tetradecapeptide (I NLKA-LAALAKKIL-NH2) phospholipase A(2) (PLA(2)) activator, mastoparan, was used to induce ACh release. Treatment of PC12 cells with appropri ate antisense oligonucleotides blocked SNAP-25 expression, as judged b y Western blot protein analysis with a specific monoclonal antibody. D espite apparent elimination of SNAP-25, treatment of differentiated PC 12 cells with mastoparan and high (80 mM) K+ induced ACh exocytosis. T he results indicate that in PC12 cells, ACh exocytosis due to mastopar an plus K+ can occur in the absence of SNAP-25.