Fine Tuning of Sympathetic Transmitter Release via Ionotropic and Metabotropic Presynaptic Receptors

2002 ◽  
Vol 54 (1) ◽  
pp. 43-99 ◽  
Author(s):  
S. Boehm
2007 ◽  
Vol 150 (1) ◽  
pp. 121-127 ◽  
Author(s):  
O Vonend ◽  
S Habbel ◽  
J Stegbauer ◽  
J Roth ◽  
L Hein ◽  
...  

1982 ◽  
Vol 242 (5) ◽  
pp. C366-C372 ◽  
Author(s):  
D. F. Wilson

The presence and physiological significance of acetylcholine (ACh) receptors on motor nerve terminals was examined at the rat diaphragm neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials (EPP), miniature end-plate potentials (MEPP), and resting potentials of the muscle fibers. Muscle action potentials were blocked by the cut-muscle technique. Quantal release was determined by the ratio EPP/MEPP, after correcting for nonlinear summation. Blockade of acetylcholinesterase with eserine and neostigmine was tested to determine the influence of residual ACh on transmitter release. Partial blockade of ACh receptors with curare was examined to further clarify the role of these presynaptic receptors. The experiments demonstrate that residual ACh inhibits transmitter release and that blockade of ACh receptors enhances transmitter release. It is concluded that presynaptic ACh receptors exist and that they serve an important physiological function. It is suggested that the presynaptic ACh receptors normally serve to limit transmitter release in a negative feedback pathway.


Drugs ◽  
1985 ◽  
Vol 29 (Supplement 2) ◽  
pp. 198-204 ◽  
Author(s):  
Eno J. Peter ◽  
Marie L. Steenberg ◽  
Mustafa F. Lokhandwala ◽  
Bhagavan S. Jandhyala ◽  
Douglas C. Eikenburg

1983 ◽  
Vol 61 (10) ◽  
pp. 1197-1201 ◽  
Author(s):  
Stanley Kalsner

The possibility of negative feedback regulation of noradrenaline release was studied in the sympathetically innervated ureters of the guinea pig mounted in vitro. Tissues were transmurally stimulated with 300 pulses at 2 Hz over a range of voltages, from 10 to 60 V. It was determined that the output of transmitter increased with increasing voltage but that the effects of supposed presynaptic antagonism by yohimbine and presynaptic agonism by added noradrenaline did not fulfill the requirements of presynaptic theory governing negative feedback. It is concluded that the presynaptic effects of these drugs is neither linked to the operation of a negative feedback system nor sensitive to the perineuronal concentrations of free and active neurotransmitter.


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