1. What is the purpose of sodium ion channels in neurons? (Be specific.)
2. How and why would blocked sodium ion channels affect excitability of a neuron?
3. What are the biological effects of tetrodotoxin on humans?
4. How and why would voltage-gated sodium channels opening at a lower voltage affect neuronal excitability?
5. If the sodium channels don't inactivate midway through an action potential, what will be the result?
6. What are the biological effects of batrachotoxin on humans?
7. How and why will blocking voltage-gated potassium channels affect neuron firing?
8. What are the biological effects of dendrotoxin on humans?
9. How and why will neuronal signaling be affected if the axon cannot release acetylcholine into the synaptic cleft?
10. What are the biological effects of botulinum toxin on humans? (Not looking for beauty tips here!)

 

Question 1

Sodium channels are responsible for the rising process of action potential in excitable cells such as neurons, myocytes, and certain forms of glia.

Question 2

Several mechanisms have been established by which the operation of voltage-gated sodium channels can be decreased by drugs and other factors. Some biological toxins, such as tetrodotoxin (a toxin found in the Fugu puffer fish), block sodium currents directly by binding to the channel pore and preventing sodium ions from flowing through the pore. "By improving the "inactivation" mechanism of these channels, lidocaine and many other clinically important drugs mainly decrease sodium channel activity. This sodium channel inactivation improvement allows the channels to become inactivated at potentials where they would usually be in the closed or resting state, which can be calculated by analyzing the channel availability voltage dependence.

The increased inactivation may also lead to a use-dependent block where in the presence of the drug, channels that are easily and repeatedly triggered are more vulnerable to inactivation. It is assumed that some of the blocking factors that may be important in inflammatory demyelinating diseases exert their effects through similar mechanisms. By directly blocking the sodium channel pore (like tetrodotoxin), by enhancing the inactivation process (like lidocaine), or by altering other sodium channel gating properties, blocking factors may affect axonal impulse transmission (perhaps preventing the closed-to-open gating transition).

Question 3

EFFECTS OF SHORT-TERM (LESS THAN 8-HOURS) EXPOSURE: Tetrodotoxin interferes by blocking sodium channels in the transmission of signals from nerves to muscles. This results in rapid muscle weakness and paralysis, including that of the respiratory tract, which can lead to death and respiratory arrest.

Question 4

?Voltage-gated ion channels are glycosylated multimeric proteins that form a potential pore that opens and closes according to the potential of the membrane, resulting in changes in membrane-wide ion flux. Four alpha subunits that make up the pore and a number of β accessory subunits have voltage-gated potassium (K+) channels. There are several different K+ pathways, and episodic ataxia or epileptic syndromes are caused by their mutations. Antibodies against one of them cause Isaacs' syndrome or acquired neuromyotonia, the dendrotoxin-sensitive fast potassium channel,

Question 5

An action potential does not occur because without voltage-dependent Na+ channels, an action potential could not be initiated in an axon. There is a step of repolarization, but now the repolarization is due to the inactivation process of Na+ alone.

Question 6

Batrachotoxin touch induces numbness in human tissue. This toxin triggers muscle and nerve depolarization, fibrillation, arrhythmias, and heart failure upon entering the body. By interfering with the body's ability to transmit electrical signals via the potential for action, BTX triggers these deadly effects.

Question 7

The movement of potassium ions through cell membranes is regulated by voltage-gated potassium canals. Activation leads to an increase in conductance, hyperpolarization, and a decline in excitability, and the termination of action potential. In comparison, a channel block contributes to depolarization, prolongation of the capacity for intervention, repeated firing, and increases in the release of transmitters and endocrine activity.

Question 8

Specific subtypes of voltage-gated potassium (K+) channels in neuronal tissue have been shown to block dendrotoxins. In the nervous system, voltage-gated K+ channels regulate the excitability of nerves and muscles by regulating the potential of the resting membrane and by repolarizing the membrane throughout the potential for action. It has been shown that dendrotoxin connects the Ranvier nodes to motor neurons and inhibits the operation of these channels of potassium. In this way, dendrotoxins extend the length of the potential for action and increase the release of acetylcholine at the neuromuscular junction, which may contribute to hyperexcitability of muscles and convulsive symptoms.

Question 9

By cleaving SNAP25, botulinum toxin blocks acetylcholine release. SNAP25 is an essential protein necessary for acetylcholine to be successfully docked and released from vesicles located in the nerve endings. A "chemical denervation" of the muscle is therefore caused by the toxin. The muscle can not contract if acetylcholine can not be released from the end of the nerve. If it is not necessary for the muscle to contract, so the overlying skin does not wrinkle.

Question 10

Botulinum toxin (Botox) is a neurotoxic protein developed by the bacterium Clostridium botulinum and related organisms. Which prevents the release of the acetylcholine neurotransmitter from the axon ends at the neuromuscular junction, causing flaccid paralysis.