Question

A virus has been sweeping through southern Arizona, causing neurological symptoms of numbness. You know that blood Na⁺, K⁺ and Ca⁺⁺ levels are normal (140, 5, 9 mequivalents per liter, respectively).

You are researchers focused on understanding how the virus is affecting neurons. You have been able to infect rats with the virus, and they also appear to experience numbness, as indicated by their lack of response to touch.

First, how could you test whether the virus was affecting just touch receptors, vs. more generalized parts of the brain, say the ascending tracts that carry the touch information, or the brain?

Second, you are able to create an in vitro preparation of the sensory neuron/touch receptors for the rat. Describe experiments that would test the hypothesis that the virus is blocking either Na⁺ or K⁺ channels in the sensory neuron.

Answer 1

When an action potential occurs, a stimulus depolarized the cell membrane and voltage-gated sodium channels open as a result. Sodium ions enter the cell to further depolarize the membrane, which opens additional sodium channels. In order to prevent a backward movement of the action potential, a refractory period occurs where the membrane was previously depolarized. This means sodium channels close for a short period of time while potassium channels open in that region. As a result, potassium ions leave the cell and the membrane is repolarized. In an unmyelinated nerve, the sodium and potassium channels are found in all areas of the axon, and an action potential travels smoothly along the length of the axon. In a myelinated nerve, Schwann cells wrap around the axon and create a myelin sheath. Myelin sheaths insulate axons by preventing ions from leaking out of the neuron. When an action potential occurs, the charge spreads down the axon until it reaches a section that is unmyelinated (node of Ranvier) and dense with sodium channels. This causes an action potential to jump down an axon much faster in a myelinated axon than in an unmyelinated axon. Myelin sheaths help transmit an action potential rapidly even if the axon has a small diameter.

If potassium channels are at fault then positive charge accumulates in the cell, since potassium ion is positively charged. Thus membrane potential difference shifts from a negative value to zero. This means depolarisation takes place.