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_JaDoreAmour _JaDoreAmour
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9 years ago
Tetrodotoxin (TTX) is a lethal neurotoxin found in the viscera of Japanese puffer fish that affects the generation of an action potential. Describe an action potential in detail and indicate the types of channels involved and the flow of ions. Finally indicate where TTX has its effects. Why is this chemical sometimes lethal?
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9 years ago
Tetrodotoxin blocks action potentials in nerves by binding to the voltage-gated, fast sodium channels in nerve cell membranes, essentially preventing any affected nerve cells from firing by blocking the channels used in the process. The binding site of this toxin is located at the pore opening of the voltage-gated Na+ channel.
Mastering in Nutritional Biology
Tralalalala Slight Smile
wrote...
9 years ago
Check this: http://en.wikipedia.org/wiki/Action_potential
Basically:
-depolarization: open voltage-operated sodium channels, slowly open voltage-operated potassium channels.
- peak: close voltage-operated sodium channels, more openning of voltage-operated potassium channels.
- repoalrization: maximum opening of voltage-operated potassium channels.
. hyperpolarization: slowly closing of voltage-operated potassium channels, but more are open than in resting.
wrote...
9 years ago
Neurons send messages electrochemically. This means that chemicals cause an electrical signal. Chemicals in the body are "electrically-charged" -- when they have an electrical charge, they are called ions. The important ions in the nervous system are sodium and potassium (both have 1 positive charge, +), calcium (has 2 positive charges, ++) and chloride (has a negative charge, -). There are also some negatively charged protein molecules. It is also important to remember that nerve cells are surrounded by a membrane that allows some ions to pass through and blocks the passage of other ions. This type of membrane is called semi-permeable.

Resting Membrane Potential

When a neuron is not sending a signal, it is "at rest." When a neuron is at rest, the inside of the neuron is negative relative to the outside. Although the concentrations of the different ions attempt to balance out on both sides of the membrane, they cannot because the cell membrane allows only some ions to pass through channels (ion channels). At rest, potassium ions (K+) can cross through the membrane easily. Also at rest, chloride ions (Cl-)and sodium ions (Na+) have a more difficult time crossing. The negatively charged protein molecules (A-) inside the neuron cannot cross the membrane.  In addition to these selective ion channels, there is a pump that uses energy to move three sodium ions out of the neuron for every two potassium ions it puts in. Finally, when all these forces balance out, and the difference in the voltage between the inside and outside of the neuron is measured, you have the resting potential. The resting membrane potential of a neuron is about -70 mV (mV=millivolt) - this means that the inside of the neuron is 70 mV less than the outside. At rest, there are relatively more sodium ions outside the neuron and more potassium ions inside that neuron.

Action Potential


The resting potential tells about what happens when a neuron is at rest. An action potential occurs when a neuron sends information down an axon, away from the cell body. Neuroscientists use other words, such as a "spike" or an "impulse" for the action potential. The action potential is an explosion of electrical activity that is created by a depolarizing current. This means that some event (a stimulus) causes the resting potential to move toward 0 mV. When the depolarization reaches about -55 mV a neuron will fire an action potential. This is the threshold. If the neuron does not reach this critical threshold level, then no action potential will fire. Also, when the threshold level is reached, an action potential of a fixed sized will always fire...for any given neuron, the size of the action potential is always the same. There are no big or small action potentials in one nerve cell - all action potentials are the same size. Therefore, the neuron either does not reach the threshold or a full action potential is fired - this is the "ALL OR NONE" principle.

Action potentials are caused when different ions cross the neuron membrane. A stimulus first causes sodium channels to open. Because there are many more sodium ions on the outside, and the inside of the neuron is negative relative to the outside, sodium ions rush into the neuron. Remember, sodium has a positive charge, so the neuron becomes more positive and becomes depolarized. It takes longer for potassium channels to open. When they do open, potassium rushes out of the cell, reversing the depolarization. Also at about this time, sodium channels start to close. This causes the action potential to go back toward -70 mV (a repolarization). The action potential actually goes past -70 mV (a hyperpolarization) because the potassium channels stay open a bit too long. Gradually, the ion concentrations go back to resting levels and the cell returns to -70 mV.

Now to answer the second part of your question:

Tetrodotoxin binds to what is known as site 1 of the fast voltage-gated sodium channel. Site 1 is located at the extracellular pore opening of the ion channel. The binding of any molecules to this site will temporarily disable the function of the ion channel. Saxitoxin, neosaxitoxin and several of the conotoxins also bind the same site.

The use of this toxin as a biochemical probe has elucidated two distinct types of voltage-gated sodium channels present in humans: the tetrodotoxin-sensitive voltage-gated sodium channel (TTX-s Na+ channel) and the tetrodotoxin-resistant voltage-gated sodium channel (TTX-r Na+ channel). Tetrodotoxin binds to TTX-s Na+ channels with a binding affinity of 5-15 nanomolar, while the TTX-r Na+ channels bind TTX with low micromolar affinity. Nerve cells containing TTX-r Na+ channels are located primarily in cardiac tissue, while nerve cells containing TTX-s Na+ channels dominate the rest of the body. The prevalence of TTX-s Na+ channels in the central nervous system makes tetrodotoxin a valuable agent for the silencing of neural activity within a cell culture.

The toxin blocks the fast Na+ current in human myocytes (the contractile cells of the muscles), thereby inhibiting their contraction. By contrast, the sodium channels in pacemaker cells of the heart are of the slow variety, so action potentials in the cardiac nodes are not inhibited by the compound. Note, the SA and AV nodes do not contain Na+ channels only Ca2+ channels, only the Purkinje fibers contain Na+ channels. The myocytes in the atrium, which surround the main cardiac pacemaker, do express this fast Na+ current and therefore the electrical activity is blocked and the heart fails to beat.
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