scholarly journals Changes in the structure of neuromuscular junctions caused by variations in osmotic pressure.

1976 ◽  
Vol 69 (3) ◽  
pp. 521-538 ◽  
Author(s):  
A W Clark

Neuromuscular junctions of the frog, Rana pipiens, were examined for structural modifications produced by exposure to increased and reduced osmotic pressure (pi). Preparations exposed to increased pi for varying lengths of time were fixed with either OSO4-Veronal with and without calcium, glutaraldehyde-phosphate, or glutaraldehyde-formaldehyde-phosphate as primary fixatives. The greatest difference between the fixatives was seen in preparations exposed to increased pi for 5 min, corresponding to the time when miniature endplate potential frequency is highest. The 5-min OSO4 calcium-free preparations appeared comparatively normal, while those fixed with OSO4 and 2 mM CaCl2 or aldehyde-phosphate had wide infoldings of the presynaptic membrane and a reduced number of synaptic vesicles. Aldehyde-phosphate had the same effect on mouse diaphragm. Another series of frog preparations were conditioned to elevated pi and then returned to normal Ringer's for varying times before fixation in OSO4-phosphate. Preparations fixed 2 min after their return to normal Ringer's showed marked disruption of the presynaptic membrane as well as apparently rupturing vesicles. If fixed after 10 min, terminals were depleted of vesicles although the presynaptic membrane had returned to its normal position and appearance.

1972 ◽  
Vol 50 (3) ◽  
pp. 279-284 ◽  
Author(s):  
D. M. J. Quastel ◽  
J. T. Hackett ◽  
K. Okamoto

Chlorpromazine, like raised osmotic pressure, not only increases spontaneous miniature endplate potential frequency (F) in mouse diaphragm (in vitro) but also depresses the slope of log F versus focal presynaptic depolarization. It also depresses the slope of log F versus [Ca], in raised K+ (constant depolarization). Similar effects are seen with pentobarbital, chloral hydrate, chloroform, and lowered pH. The drugs have similar actions in locust muscle, where the transmitter is not acetylcholine.


2009 ◽  
Vol 513 (5) ◽  
pp. 457-468 ◽  
Author(s):  
Sharuna Nagwaney ◽  
Mark Lee Harlow ◽  
Jae Hoon Jung ◽  
Joseph A. Szule ◽  
David Ress ◽  
...  

1991 ◽  
Vol 104 (4) ◽  
pp. 1024-1032 ◽  
Author(s):  
E.E. Nikolsky ◽  
E.A. Bukharaeva ◽  
E.G. Strunsky ◽  
F. Vyskočil

1980 ◽  
Vol 85 (2) ◽  
pp. 337-345 ◽  
Author(s):  
R Fesce ◽  
F Grohovaz ◽  
W P Hurlbut ◽  
B Ceccarelli

The intramembrane particles on the presynaptic membrane and on the membrane of synaptic vesicles were studied at freeze-fractured neuromuscular junctions of the frog. The particles on the P face of the presynaptic membrane belong to two major classes: small particles with diameters less than 9 nm and large particles with diameters between 9 and 13 nm. In addition, there were a few extralarge particles with diameters greater than 13 nm. Indirect stimulation of the muscle, or the application of black widow spider venom, decreased the concentration of small particles on the presynaptic membrane but did not change the concentration of large particles. Three similar classes of particles were found on the P face of the membrane of the synaptic vesicles. The concentrations of large and extralarge particles on the vesicle membrane were comparable to the concentrations of these particles on the presynaptic membrane, whereas the concentration of small particles on the vesicle membrane was less than than the concentration of small particles on the presynaptic membrane. These results are compatible with the idea that synaptic vesicles fuse with the presynaptic membrane when quanta of transmitter are released. However, neither the large nor the extralarge particles on the P face of the presynaptic membrane can be used to trace the movement of vesicle membrane that has been incorporated into the axolemma.


1. Electrophysiological and electron-microscopic studies were made of the effect of lan­thanum ions on frog neuromuscular junctions. 2. In the presence of 1 mM La 2+ , nerve impulses continued to invade the nerve terminals but ceased to release transmitter. 3. Lanthanum caused a rapid and large increase in the frequency of miniature end-plate potentials; presumably because La activates the mechanism of transmitter release without the usual prerequisite of presynaptic membrane depolarization. At 4 °C, La caused a 10000-fold, or even larger increase in the rate of leakage of transmitter quanta. Such high rate of trans­mitter release was not accompanied by obvious changes in electron-microscopic structure of the nerve terminals. 4. With continued La-treatment, the frequency of miniature end-plate potentials subsides slowly until they are no longer detectable at most end-plates. During this period the number of synaptic vesicles is reduced until practically all the endings become completely depleted of synaptic vesicles. In contrast, coated vesicles and membrane-bound tubes and cysternae become more numerous.


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