Effects of hypertonic solutions on quantal transmitter release at the crayfish neuromuscular junction

Abstract

SUMMARY1. The effects ofa hypertonic bathing medium, containing either NaCl or melezitose, on the average number (m) and the time course of quantal release following an action potential were studied using focal extracellular recording methods at synaptic sites on the opener muscle of the crayfish leg.2. After the application of hypertonic saline, the rate of spontaneous quantal release increased but m decreased to a new level within 1 min; the extent of depression depended on the magnitude of the increase in tonicity until the osmolarity was 50 % greater than the normal value of 0 43 osmol/l (Osm), but greater increases in tonicity exerted little further effect. 3. The synaptic delays were increased and distributed over a longer range of time in hypertonic solutions; also, the latency between the first and second quantal releases in a multiple response to a single nerve impulse was also increased.4. Hypertonicity had no significant effect on the conduction velocity of the action potential, the independence of successive quantal releases in the same response, or the uniformity of the rise and fall of the probability of quanta release following an action potential, a(t).5. The time course of a(t) is prolonged in hypertonic solutions; this was manifested as an increase in the time constant of the exponential decline in a(t) from its peak value following the nerve impulse.5. When the potentiating agent 5-hydroxytryptamine (5-HT) was added to the hypertonic saline, m was increased, and the time course of a(t) was prolonged further than in the hypertonic solution alone; 5-HT produced no change in the time course of a(t) when it was added to normal saline, although m was increased.6. It is concluded that in this preparation hypertonicity decreases the rate of release of each quantum from the nerve terminal following a nerve impulse.

UNC-13 is required for synaptic vesicle fusion in C. elegans

“…The nIs52 array includes a construct with GFP fused to the lumenal terminus of the synaptic vesicle protein synaptobrevin, under the regulation of the unc-25 promoter, which is expressed in GABAergic neurons 17 . Primed vesicles can be induced to fuse with the plasma membrane in the absence of calcium influx by application of hyperosmotic media [21][22][23] , and the SNARE complex is required for vesicle fusion induced in this way 11 . To determine whether the docked vesicles we observed in electron micrographs were fusion competent, we applied hyperosmotic media to unc-13 mutants.…”

The calcium dependence of spontaneous and evoked quantal release at the frog neuromuscular junction

“…Note added in proof. Niles & Smith (1982) studied the effects of hypertonic solutions on spontaneous and evoked quantal release at the crayfish neuromuscular junction. They found that hypertonic solutions, ranging from 04 to 1-3 Osm, decreased evoked output, m, but increased the rate of spontaneous quantal release.…”

Fusion of phospholipid vesicles with a planar membrane depends on the membrane permeability of the solute used to create the osmotic pressure.

“…This method of swelling is routinely used to reconstitute ion channels into planar membranes via fusion (Moczydlowski et al, 1985). In a wide range of biological secretory systems, osmoticants have been added to cells to shrink granules, and fusion has been inhibited (Niles and Smith, 1982;Zimmerberg and Whitaker, 1985;Holz, 1986).…”