Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 565, Issue 3, Pages 743-750Publisher
WILEY
DOI: 10.1113/jphysiol.2005.087296
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Funding
- NINDS NIH HHS [R01 NS024752, R37 NS024752, NS-24752] Funding Source: Medline
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At the snake neuromuscular junction, low temperature (LT, 5-7 degrees C) blocks clathrin-mediated endocytosis (CME) while exocytosis is largely unaffected. Thus compensatory endocytosis that normally follows transmitter release is inhibited, or 'delayed' until the preparation is warmed to room temperature (RT). This delay was exploited to observe how changes in bulk [Ca2+](i) directly affect CME. Motor terminals were loaded with fura-2 to monitor [Ca2+](i). With brief stimulation at LT, [Ca2+](i), transiently increased but returned to baseline (similar to 63 nm) in < 8 min. After 15 min at LT, [Ca2+](i) was altered by incubating preparations in the Ca2+ ionophore ionomyocin. Preparations were then warmed to RT to initiate delayed endocytosis, which was quantified as uptake of the fluorescent optical probe sulforhodamine 101. Endocytosis was more rapid when [Ca2+](i) increased; the rate at 300 nm Ca2+ was similar to double that under basal conditions. Thus the rate of CME - isolated from stimulation, transmitter release, and other forms of endocytosis-is directly influenced by intraterminal Ca2+.
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