Double mode of action of black widow spider venom on frog neuromuscular junction

1978 ◽  
Vol 7 (2) ◽  
pp. 193-205 ◽  
Author(s):  
Alfredo Gorio ◽  
Lee L. Rubin ◽  
Alexander Mauro
Keyword(s):  
Neuromuscular Junction ◽  
Mode Of Action ◽  
Spider Venom ◽  
Frog Neuromuscular Junction ◽  
Black Widow ◽  
Black Widow Spider ◽  
Black Widow Spider Venom ◽  
Widow Spider

scholarly journals Reversibility and mode of action of Black Widow spider venom on the vertebrate neuromuscular junction.

1979 ◽  
Vol 73 (2) ◽  
pp. 245-263 ◽  
Author(s):  
A Gorio ◽  
A Mauro
Keyword(s):  
Nerve Ending ◽  
Mode Of Action ◽  
Neuromuscular Junctions ◽  
Divalent Cations ◽  
Normal Function ◽  
Spider Venom ◽  
Black Widow ◽  
Black Widow Spider ◽  
Black Widow Spider Venom ◽  
Widow Spider

Black widow spider venom (BWSV) stimulates transmitter release and depletes synaptic vesicles from muscles bathed in a sodium free medium containing 1 mM EGTA. However, frog neuromuscular junctions treated with BWSV in glucosamine Ringer's and post-treated with antivenin recover normal function. This suggests that probably the permanent block of neuromuscular transmission is due to changes in permeability of the nerve ending plasma membrane to cations such as Na+. When BWSV is applied in a medium lacking divalent cations and containing 1 mM EGTA, in most of the cases no effect is observed. We found that this inhibition can be overcome in three ways: (a) by adding divalent cations to the medium; (b) by increasing the tonicity of the medium with sucrose; (c) by raising the temperature of the medium. These results suggest that the lack of divalent cations influences the membrane fluidity. Moreover, in view of the report by Yahara and Kakimoto-Sameshima (1977. Proc. Natl. Acad. Sci. U.S.A. 74:4511--4515) that hypertonic media induce capping of surface receptors in lymphocytes and thymocytes, we think that these data further support the hypothesis that BWSV stimulates release by a dual mode of action; namely, it increases the nerve ending permeability to cations and also stimulates release directly via a process of redistribution of membrane components, a process which may also inhibit vesicle recycling.

scholarly journals CHANGES IN THE FINE STRUCTURE OF THE NEUROMUSCULAR JUNCTION OF THE FROG CAUSED BY BLACK WIDOW SPIDER VENOM

1972 ◽  
Vol 52 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Allen W. Clark ◽  
William P. Hurlbut ◽  
Alexander Mauro
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Synaptic Vesicles ◽  
Spider Venom ◽  
Presynaptic Membrane ◽  
Black Widow ◽  
Black Widow Spider ◽  
End Plate ◽  
Black Widow Spider Venom ◽  
Widow Spider

Application of black widow spider venom to the neuromuscular junction of the frog causes an increase in the frequency of miniature end-plate potentials (min.e.p.p.) and a reduction in the number of synaptic vesicles in the nerve terminal. Shortly after the increase in min.e.p.p. frequency, the presynaptic membrane of the nerve terminal has either infolded or "lifted." Examination of these infoldings or lifts reveals synaptic vesicles in various stages of fusion with the presynaptic membrane. After the supply of synaptic vesicles has been exhausted, the presynaptic membrane returns to its original position directly opposite the end-plate membrane. The terminal contains all of its usual components with the exception of the synaptic vesicles. The only other alteration of the structures making up the neuromuscular junction occurs in the axon leading to the terminal. Instead of completely filling out its Schwann sheath, the axon has pulled away and its axoplasm appears to be denser than the control. The relation of these events to the vesicle hypothesis is discussed.

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