Exocytosis In Terminals Research Articles

Extending the realm of membrane capacitance measurements to nerve terminals with complex morphologies

Extending the realm of membrane capacitance measurements to nerve terminals with complex morphologies

Depletion of calcium stores regulates calcium influx and signal transmission in rod photoreceptors

Tonic synapses are specialized for sustained calcium entry and transmitter release, allowing them to operate in a graded fashion over a wide dynamic range. We identified a novel plasma membrane calcium entry mechanism that extends the range of rod photoreceptor signalling into light-adapted conditions. The mechanism, which shares molecular and physiological characteristics with store-operated calcium entry (SOCE), is required to maintain baseline [Ca(2+)](i) in rod inner segments and synaptic terminals. Sustained Ca(2+) entry into rod cytosol is augmented by store depletion, blocked by La(3+) and Gd(3+) and suppressed by organic antagonists MRS-1845 and SKF-96365. Store depletion and the subsequent Ca(2+) influx directly stimulated exocytosis in terminals of light-adapted rods loaded with the activity-dependent dye FM1-43. Moreover, SOCE blockers suppressed rod-mediated synaptic inputs to horizontal cells without affecting presynaptic voltage-operated Ca(2+) entry. Silencing of TRPC1 expression with small interference RNA disrupted SOCE in rods, but had no effect on cone Ca(2+) signalling. Rods were immunopositive for TRPC1 whereas cone inner segments immunostained with TRPC6 channel antibodies. Thus, SOCE modulates Ca(2+) homeostasis and light-evoked neurotransmission at the rod photoreceptor synapse mediated by TRPC1.

Evidence against the swelling hypothesis for initiation of exocytosis in terminals of chromaffin cell processes

Exocytosis of transmitter-containing granules was directly visualized in neurite terminals of cultured chromaffin cells under a video-enhanced contrast microscope. The granule diameter did not change immediately before their exocytotic responses. Large granules responded as early as small ones. These findings are inconsistent with the swelling hypothesis for initiation of exocytosis.

Ultrastructural dynamics of exocytosis in the ovulation-neurohormone producing caudo-dorsal cells of the freshwater snail Lymnaea stagnalis (L.).

The ultrastructural dynamics of exocytosis in the ovulation-stimulating neurosecretory Caudo-Dorsal Cells (CDC) of the freshwater snail L. stagnalis were studied after incubation of cerebral ganglia in Ringer's solutions with different concentrations of K+ and Ca2+. Detection of exocytosis was facilitated by the use of the tannic acid-glutaraldehyde fixation method (TAGO-method). In control Ringer (low K+) the frequency of exocytosis was rather low. Exocytosis mainly occurred as "terminal" exocytosis (TE); "intracellular" (ICE) and, particularly, "multiple" exocytosis (ME) took place infrequently. Incubation in high K+-containing Ringer strongly increased exocytotic activity. Compared to the controls the total frequency of exocytosis was 50 X as high, whereas TE, ICE and ME occurred 6 X, 47 X, and more than 300 X as frequently, respectively. In high K+/Ca2+-free Ringer the total frequency of exocytosis was only 2 X as high as in control Ringer. It is concluded that TE, ICE, and ME are normal, Ca2+-dependent exocytotic phenomena. The significance of their dynamics in response to K+-stimulation is discussed. The extremely high frequency of exocytosis, as well as the presence of "unaltered granule contents in transit", is explained by assuming that an exocytotic event in the CDC lasts rather long, viz. some minutes. The results may reflect the physiological mechanism by which the CDC release their ovulation hormone. The possible involvement of "clear" and "large" electron lucent vesicles in membrane reuptake after exocytosis is considered.