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How Does Ttx Affect Action Potential



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Question
what would happen if your potassium channels do not open?
if your sodium channels open and your potassium channels do not

Answer
The Role of the Sodium–Potassium Exchange Pump In an action potential, depolarization results from the influx of Na+ and repolarization involves the loss of K+. Over time, the sodium–potassium exchange pump returns intracellular and extracellular ion concentrations to prestimulation levels. Compared with the total number of ions inside and outside the cell, however, the number involved in a single action potential is insignificant. Tens of thousands of action potentials can occur before intracellular ion concentrations change enough to disrupt the entire mechanism. Thus the exchange pump is not essential to any single action potential. However, a maximally stimulated neuron can generate action potentials at a rate of 1000 per second. Under these circumstances, the exchange pump is needed if ion concentrations are to remain within acceptable limits over a prolonged period. The sodium–potassium exchange pump requires energy in the form of ATP. Each time the pump exchanges two extracellular potassium ions for three intracellular sodium ions, one molecule of ATP is broken down to ADP. The transmembrane protein of the exchange pump is called sodium–potassium ATPase because it splits ATP to ADP. If sodium–potassium ATPase is inactivated by a metabolic poison or if the cell runs out of ATP, a neuron will soon lose its ability to function. Finally, Neurotoxins: Potentially deadly forms of poisoning result from eating seafood containing neurotoxins, poisons that affect primarily neurons. Several neurotoxins, such as tetrodotoxin (TTX), prevent sodium from entering voltage-regulated sodium channels. The result is an inability to generate action potentials. Motor neurons cannot function under these conditions, and death by suffocation can result from paralysis of the respiratory muscles. -Birdy



Question
Nervous System Q's?
Do Axons Grow back in the PNS or CNS? How do neuro-toxins work? (give a link if necessary)

Answer
PNS is better. The ability of the CNS to generate new neurons or to repair axons following trauma is very limited, especially when compared to the abilities of the PNS. Depends on the neurotoxin. Many neurotoxins act by affecting voltage-dependent ion channels, such as tetrodotoxin (TTX). This chemical acts to block sodium channels in neurons, preventing action potentials. This leads to paralysis and eventually death.



Question

Answer
When threatened, Pufferfish can inflate their body by swallowing water to increase their apparent size to deter predators. In addition some puffers produce an extremely poisonous toxin called anhydrotetrodotoxin 4-epitetrodotoxin and is over a 1,000 times more poisonous than potassium cyanide, this toxin is found in the skin, liver, and gonads. Tetrodotoxin (TTX) is produced by a bacterium, Pseudoalteromonas haloplanktis tetraodonis. This bacteria lives in the body of certain species, most notably the pufferfish, Fugu xanthopterus, but is also known as teppo, fugu, or blowfish. As a painkiller, TTX has been shown to be 3200 times stronger than morphine but with few side effects. This potential addition to the analgesic market will benefit those who cannot take the current painkillers, or have become addicted. TTX promises to be powerful, yet non-addictive. When administered, the patient receives only several micrograms, a very tiny quantity. This seems to be operating on principles used in homeopathy, where much diluted substances are delivered. Because it interferes with the nerves ability to send messages to the brain, patients then don’t ‘feel’ the pain. The formula for tetrodotoxin, is C11H17N3O8. The relative proportions are C 41.38%, H 5.37%, N 13.16% and O 40.09%. It is otherwise known as Octahydro-12-(hydroxymethyl)-2-imino-5,9:7,10a-dimethano-10aH-[1,3]dioxocino[6,5-d]pyrimidine-4,7,10,11,12-pentol; Tetrodotoxin; and Tetrodotoxin, citrate free. One unique characteristic of TTX is its guanidinium moiety, which is a key binding site for sodium and other molecules. MODE OF HARMFUL ACTION IN HUMANS. There is no antidote to poisoning to this poison. (TTX) is referred to in the literature as a maculotoxin, tarichatoxin, tetrodontoxin, fugu poison and spheriodine. Anhydrotetrodotoxin, Araregai toxin, 4-Epitetrodotoxin, and Tetrodonic acid are also names used in literature A maculotoxin causes visual impairment, even blindness. The blue ringed octopus is often cited as an example of this toxin. The other names, tarichatoxin, refers to another source of the poison, the genus of amphibious newts (Taricha). The name tetrodontoxin seems to be an alternate spelling, referring to ‘Tetradon’ the genus of many puffer fish, and is used in foreign literature. 10,000 times more potent than cyanide, paralysis is its mode of action, and is evident as early as 20 minutes after exposure Most fatalities have occurred after eating fugu, the meat of the pufferfish. The description of what happens to people who are being poisoned by TTX is unbelievable. There is some consideration that the source of the notion of ‘zombies’ might come from such a poisoning. Since people who exhibit such poisoning go through stages, ending up unable to move, there is some documentation that some people have been buried alive, thought to be dead because of their unresponsive nature due to the poisoning. Some literature mentions that one reason the Japanese keep the deceased for 3 days prior to burial is to avoid such accidental burials. A slight numbness in the lips and tongue commences the first signs of poisoning. The numbness soon increases and spreads to certain parts of your face and throat; also involuntary muscle spasms, weakness, dizziness, and loss of speech ensues. Excessive salivation and sweating, along with slowed heart rate and a drop in body temperature come next. Respiratory distress, marked by rapid, shallow breathing is soon followed by the secondary stage of the poisoning. This involves increased paralysis, to the point where even sitting becomes difficult, mental impairment and convulsions and then cardiac arrhythmia. Because tetrodotoxin doesn't cross the brain-blood barrier it is not directly affected by this toxin. There have been reports of “fugu poisoning survivors that they were completely lucid during the entire event, finally recovering to tell the tale.” Upon exposure, TTX bind to specific sodium channels on the nerve cells, stopping the flow of sodium into the cells and causing the nerves to stop functioning, causing paralysis and death. Nerves cannot send messages to the muscles, because the connection has been ‘unplugged.’ closed, or made inactivate, spontaneously even though the membrane potential remains at the level which opened them. Na channels are found in neurons, vertebrate skeletal muscle, and cardiac muscle. They serve to let positive charge into the cell. Na channels are used in places where you need fast, reliable voltage changes, such as when propagating an action potential down an axon. Na serves to let charge into the cell; the Na itself doesn't do anything chemically. The puffer fish and other similar species have a mutated version of the sodium channel receptor that makes it immune to the toxin. This arrangement allows for a symbiotic relationship to exist between the puffer and bacteria, in return for manufacturing their deadly toxin to keep their hosts safe from predators, the bacteria are afforded a home inside the puffer.




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