Search results
Results from the WOW.Com Content Network
The main toxin of curare, d-tubocurarine, occupies the same position on the receptor as ACh with an equal or greater affinity, and elicits no response, making it a competitive antagonist. The antidote for curare poisoning is an acetylcholinesterase (AChE) inhibitor (anti-cholinesterase), such as physostigmine or neostigmine. By blocking ACh ...
Curare was found to block the stimulant action of nicotine in both innervated and chronically denervated muscles. In 1940, Jenkinson identified tubocurarine as a competitive antagonist of acetylcholine. Curare and tubocurarine had important roles in establishing the concept of specific cholinoceptors in the motor end plate. [3]
Neuromuscular junction diseases in this category include snake venom poisoning, botulism, arthropod poisoning, organophosphates and hypermagnesemia.(reference 13) Organophosphates are present in many insecticides and herbicides. They are also the basis of many nerve gases.(reference 27) Hypermagnesmia is a condition where the balance of ...
The neurotransmitter, acetylcholine(ACh) binds to the nicotinic receptors on the motor end plate, which is a specialised area of the muscle fibre's post-synaptic membrane. This binding causes the nicotinic receptor channels to open and allow the influx of Na + into the muscle fibre. [17]
Tubocurarine is so-called because some of the plant extracts designated curare were stored, and subsequently shipped to Europe, in bamboo tubes. Likewise, curare stored in calabash containers was called calabash curare, although this was usually an extract not of Chondrodendron, but of the Strychnos species S. toxifera , containing a different ...
The "Dr. X" killings were a series of suspicious deaths by curare poisoning, in 1966 at a Bergen County, New Jersey hospital. [1] A newspaper investigation during the mid-1960s led to the indictment of an Argentina-born physician, Mario Enrique Jascalevich (August 27, 1927 — September 1984), in 1976. He was acquitted at trial in 1978.
Signal transmission from nerve to muscle at the motor end plate. The neuromuscular junction is the synapse that is formed between an alpha motor neuron (α-MN) and the skeletal muscle fiber. In order for a muscle to contract, an action potential is first propagated down a nerve until it reaches the axon terminal of the motor neuron.
Tetraethylammonium (TEA) is a compound that, like a number of neurotoxins, was first identified through its damaging effects to the nervous system and shown to have the capacity of inhibiting the function of motor nerves and thus the contraction of the musculature in a manner similar to that of curare. [58]