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Rapid exocytosis and endocytosis in nerve terminals of the rat posterior pituitary.
Author(s) -
Hsu S F,
Jackson M B
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021512
Subject(s) - exocytosis , depolarization , capacitance , endocytosis , biophysics , membrane potential , chemistry , vesicle , time constant , membrane , biology , electrode , biochemistry , cell , engineering , electrical engineering
1. Ca(2+)‐induced exocytosis and endocytosis were studied by measuring the membrane capacitance of voltage‐clamped peptidergic nerve terminals in slices prepared from the rat posterior pituitary. 2. Depolarizing pulses produced rapid increases in capacitance. These increases varied in parallel with Ca2+ current as voltage was varied. Elimination of Ca2+ current blocked depolarization‐induced capacitance changes. 3. Depolarization‐induced capacitance changes increased with pulse duration. Capacitance changes also increased with integrated Ca2+ influx, but saturated at high levels of Ca2+ entry. This saturation allowed us to estimate a pool size of 190 vesicles, assuming each vesicle has a capacitance of 1 fF. Vesicles from this pool fused with a time constant of 0.43 s. The capacitance change increased with the first power of integrated Ca2+ influx. 4. Experiments with briefer pulses revealed a rapid component of exocytosis comprising a pool of forty vesicles that fuse with a time constant of 14 ms. This rapid process may reflect a final Ca(2+)‐regulated triggering step, which is distinct from the slower kinetic step revealed by longer duration pulses. The slower step may reflect a priming of vesicles prior to exocytosis. 5. Depolarization‐induced capacitance increases in most cases were followed by a rapid decay in capacitance, reflecting membrane reuptake tightly coupled to exocytosis. A variable amount of rapid endocytosis followed depolarization‐induced capacitance increases. The time constant for rapid endocytosis to baseline was 0.44 s. Excess endocytosis was occasionally observed, with capacitance decaying below the pre‐stimulus baseline with a time constant of 2.1 s. 6. Rapid endocytosis was slower after pulses that produced greater increases in intracellular Ca2+, consistent with the hypothesis that intracellular Ca2+ inhibits rapid endocytosis. 7. Exocytosis follows depolarization with no detectable delay, indicating that Ca2+ triggers neuropeptide secretion from nerve terminals with kinetics comparable to that observed in other rapidly secreting systems.