scholarly journals The effects of nerve terminal activity on non-quantal release of acetylcholine at the mouse neuromuscular junction.

1990 ◽  
Vol 423 (1) ◽  
pp. 631-640 ◽  
Author(s):  
H Zemková ◽  
F Vyskocil ◽  
C Edwards
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Quantal Release ◽  
Release Of Acetylcholine

Coated vesicles and pits during enhanced quantal release of acetylcholine at the neuromuscular junction

1987 ◽  
Vol 16 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Francesca Torri-Tarelli ◽  
Claudia Haimann ◽  
Bruno Ceccarelli
Keyword(s):  
Neuromuscular Junction ◽  
Coated Vesicles ◽  
Quantal Release ◽  
Release Of Acetylcholine

scholarly journals Augmented quantal release of acetylcholine at the vertebrate neuromuscular junction following tdp-43 depletion

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0177005 ◽  
Author(s):  
Stefania Dzieciolowska ◽  
Pierre Drapeau ◽  
Gary Alan Barclay Armstrong
Keyword(s):  
Neuromuscular Junction ◽  
Quantal Release ◽  
Release Of Acetylcholine

Persistence of Synaptic Vesicles After Photodynamic Abolition of Quantal Release at the Neuromuscular Junction of the Lizard

1985 ◽  
Vol 43 ◽  
pp. 698-699
Author(s):  
G. D. Pappas ◽  
A. L. Politoff ◽  
W. Lifschitz ◽  
V. Kriho
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Rose Bengal ◽  
Synaptic Vesicles ◽  
Presynaptic Terminal ◽  
Physiological Effects ◽  
Quantal Release ◽  
End Plate ◽  
Photic Stimulus

We have used rose bengal (RB) to study the ultrastructural and physiological effects of in vivo photooxidation of the presynaptic terminal of the neuromuscular junction. Rose bengal (RB) is a powerful xanthine photosensitizer capable of inducing fairly selective photooxidation of histidinyl residues of proteins when exposed to light in the present of O2 (from air) and pH near 7.0. Recent observations by Politoff and Lifschitz show that RB is taken up spontaneously by the nerve terminal and selectively accumulated in the presynaptic region; after uptake of RB, illumination of the presynaptic region with a microscopic photic stimulus (1.3 x 103 erg) causes a brief (15 min) and small burst (3.0 x 103 total release) of miniature end plate potentials (m.e.p.p.), followed by total abolition of m.e.p.p.'s, in spite of preservation of postsynaptic sensitivity.

Dependence on multivalent cations of quantal release of transmitter induced by black widow spider venom

1987 ◽  
Vol 253 (3) ◽  
pp. C469-C476 ◽  
Author(s):  
S. Misler ◽  
L. C. Falke
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Divalent Cations ◽  
Spider Venom ◽  
Trivalent Cation ◽  
Black Widow ◽  
Black Widow Spider ◽  
Quantal Release ◽  
Black Widow Spider Venom ◽  
Widow Spider

Application of alpha-latrotoxin (alpha-LT), the active component of black widow spider venom (BWSV), to a vertebrate neuromuscular junction, in the presence of millimolar bath concentrations of Ca2+ or Mg2+, greatly increases the frequency of miniature end-plate potentials (Fmepp). We have further characterized the cation dependence of alpha-LT action at the frog cutaneous pectoris neuromuscular junction. The divalent cations, Ca, Sr, Ba at less than or equal to 50 microM, Zn, Mn, Cd at greater than or equal to 50-100 microM, and Mg at greater than or equal to 1.0 mM, as well as the trivalent cation La at greater than or equal to 15 microM, all increase Fmepp exponentially to greater than or equal to 100-200 s-1 over several minutes time. The exponential rate of rise is graded with extracellular cation concentration and can be reduced by increasing [K+] of the bath from 2 to 25-40 mM. Long-term exposure to alpha-LT in the presence of Sr2+ or Mn2+ results in the exhaustion of the releasable quantal store of transmitter, which in the case of Mn2+ correlates well with depletion of synaptic vesicles. These data support the hypothesis that BWSV promotes an increase in Fmepp by increasing nerve terminal permeability to multivalent cations that enter the nerve terminal down their electrochemical gradients and then may bind to quantal release activating sites or displace Ca2+ from intracellular stores.

scholarly journals Glutamate regulation of non-quantal release of acetylcholine in the rat neuromuscular junction

2003 ◽  
Vol 85 (1) ◽  
pp. 206-213 ◽  
Author(s):  
Artem I. Malomouzh ◽  
Marat R. Mukhtarov ◽  
Eugen E. Nikolsky ◽  
František Vyskočil ◽  
Edward M. Lieberman ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Quantal Release ◽  
Release Of Acetylcholine

Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat

1999 ◽  
Vol 22 (12) ◽  
pp. 1660-1666 ◽  
Author(s):  
Jonathan P. Edwards ◽  
Paul A. Hatton ◽  
Roderick A. Little ◽  
Richard A. Pennington ◽  
Anthony C. Wareham
Keyword(s):  
Neuromuscular Junction ◽  
Quantal Release ◽  
Scald Injury ◽  
Release Of Acetylcholine
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