INCORPORATION OF SYNAPTOTAGMIN-II TO THE AXOLEMMA OF BOTULINUM TYPE-APOISONED MOUSE MOTOR ENDINGS DURING ENHANCED QUANTAL ACETYLCHOLINE-RELEASE

The involvement of terminal sprouts in neurotransmitter release by in vivo botulinum type-A toxin poisoned motor endings was investigated 15 to 40 days after a single injection of the toxin onto the levator aur is longus muscle of the mouse. Enhanced quantal acetylcholine release was induced by a-latrotoxin or La3+ in conditions that prevent endocyt osis, and an antibody directed against the lumenal domain of synaptota gmin Il (Syt Il) was used in the presence or absence of Triton X-100. We showed that, under resting conditions, the intravesicular domain of Syt Il requires Triton X-100 to be labelled, whereas it becomes expos ed to the outside of the axolemma of both the original terminal arbori zation and the newly formed sprouts during enhanced exocytosis. These data were taken to indicate that, when sprouting is prominent, the who le modified terminal arborization, including the original branches and the sprouts, possesses the machinery for Ca2+-independent exocytosis. (C) 1998 Elsevier Science:B.V. All rights reserved.