α-Bungarotoxin, κ-bungarotoxin, α-cobratoxin and erabutoxin-b do not affect [3H]acetylcholine release from the rat isolated left hemidiaphragm

1995 ◽  
Vol 352 (6) ◽  
pp. 646-652 ◽  
Author(s):  
C. Apel ◽  
J. Říčný ◽  
G. Wagner ◽  
I. Wessler
2012 ◽  
Vol 21 (1) ◽  
pp. 15-21
Author(s):  
Merete Bakke ◽  
Allan Bardow ◽  
Eigild Møller

Severe drooling is associated with discomfort and psychosocial problems and may constitute a health risk. A variety of different surgical and non-surgical treatments have been used to diminish drooling, some of them with little or uncertain effect and others more effective but irreversible or with side effects. Based on clinical evidence, injection with botulinum toxin (BTX) into the parotid and submandibular glands is a useful treatment option, because it is local, reversible, and with few side effects, although it has to be repeated. The mechanism of BTX is a local inhibition of acetylcholine release, which diminishes receptor-coupled secretion and results in a flow rate reduction of 25–50% for 2–7 months.


1964 ◽  
Vol 48 (6) ◽  
pp. 912-920 ◽  
Author(s):  
Jens G. Rosenkrantz ◽  
Ernest K. Cotton ◽  
William R. Waddell

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mouzarllem B. Reis ◽  
Fernanda L. Rodrigues ◽  
Natalia Lautherbach ◽  
Alexandre Kanashiro ◽  
Carlos A. Sorgi ◽  
...  

Abstract Scorpion envenomation is a leading cause of morbidity and mortality among accidents caused by venomous animals. Major clinical manifestations that precede death after scorpion envenomation include heart failure and pulmonary edema. Here, we demonstrate that cardiac dysfunction and fatal outcomes caused by lethal scorpion envenomation in mice are mediated by a neuro-immune interaction linking IL-1 receptor signaling, prostaglandin E2, and acetylcholine release. IL-1R deficiency, the treatment with a high dose of dexamethasone or blockage of parasympathetic signaling using atropine or vagotomy, abolished heart failure and mortality of envenomed mice. Therefore, we propose the use of dexamethasone administration very early after envenomation, even before antiserum, to inhibit the production of inflammatory mediators and acetylcholine release, and to reduce the risk of death.


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