Biology Question

Question

1. Explain how your brain perceives the location and intensity of a stimulus like pain. (1 pt)

2. Say you are looking at a neuron with a higher concentration of K+ ions inside the cell than outside. When K+ channels are open, why is there no net diffusion of K+ ions across the membrane even though there is a large concentration difference inside vs outside cell? (2 pts)

3. There is a type of algae that create a red tide algal bloom in coastal waters. These algae also release a toxin that acts by blocking voltage-gated sodium channels, and some species of clams are affected by this toxin. Describe what effect this toxin would have on the clams and why. (2 pts)

4. Describe the movement of Na+ and K+ ions and the changes in Vm during the phases of an action potential [at rest, depolarization, repolarization/hyperpolarization, after hyperpolarization]. Include the opening and closing of voltage-gated sodium and potassium channels in each step.

Hint: complete the puzzle on p. 12 in the tutorial. (2 pts)

5. Describe the role of myelin in action potential propagation and why the loss of myelin (for example, through multiple sclerosis) can lead to symptoms such as loss of motor control. (1 pt)

Answer 1

When a stimulus like pain is detected by the sensory receptors, it is transmitted through the nervous system to the brain, where it is processed and perceived. The location of the stimulus is determined by the sensory receptors that are activated, and the intensity of the stimulus is determined by the frequency and number of action potentials generated by the sensory neurons. The brain integrates this information from multiple sensory modalities to create a spatial representation of the stimulus and a perception of its intensity.

When K+ channels are open, there is no net diffusion of K+ ions across the membrane because the membrane potential (Vm) is close to the equilibrium potential (EK) for K+. At rest, the K+ channels are closed, and the Vm is maintained by the activity of Na+/K+ pumps, which actively transport Na+ out of the cell and K+ into the cell, against their concentration gradients. When the K+ channels open, K+ ions move out of the cell, but this movement is counterbalanced by the diffusion force that drives K+ ions back into the cell, due to the negative Vm. Therefore, there is no net movement of K+ ions across the membrane.

The toxin released by the red tide algae that blocks voltage-gated sodium channels would prevent the generation and propagation of action potentials in the affected clams. Voltage-gated sodium channels are required for the rapid depolarization phase of the action potential, which allows for the transmission of electrical signals along the axons of neurons and muscle cells. The blockage of these channels would lead to a reduction in the excitability and function of the affected cells, potentially leading to paralysis or death.

At rest, the neuron has a negative Vm, maintained by the Na+/K+ pumps and the passive diffusion of K+ ions out of the cell through leak channels. During depolarization, the Vm becomes less negative and approaches the threshold potential, due to the opening of voltage-gated sodium channels that allow Na+ ions to enter the cell, creating a positive feedback loop that further depolarizes the membrane. During repolarization and hyperpolarization, the Vm returns to the resting potential, due to the opening of voltage-gated potassium channels that allow K+ ions to leave the cell, and the closing of voltage-gated sodium channels. After hyperpolarization, the Vm briefly becomes more negative than the resting potential, before returning to the resting potential. The opening and closing of these channels are controlled by changes in the membrane potential, with voltage-gated sodium channels opening at the threshold potential and voltage-gated potassium channels opening and closing more slowly, following the depolarization phase.

Myelin is a fatty sheath that surrounds the axons of neurons, allowing for faster conduction of action potentials by increasing the membrane resistance and reducing the capacitance of the axonal membrane. The loss of myelin, as in the case of multiple sclerosis, can lead to symptoms such as loss of motor control, due to the slowing and disruption of action potential propagation along the affected axons. The demyelinated axons are more susceptible to depolarization block, in which the frequency of action potentials is reduced or blocked altogether, due to the excessive buildup of extracellular potassium ions that cannot be rapidly cleared by the slow Na+/K+ pumps. This can lead to the failure of action potential transmission and a loss of neural function.