A deficit of which ion in the extracellular fluid can cause nerve fibers to become highly excitable, sometimes leading to spontaneous discharge and muscle tetany?
Explanation
This question tests the understanding of the stabilizing role of extracellular calcium ions on voltage-gated sodium channels and the clinical consequence of its deficit.
Other questions
What is the primary cause for the establishment of a membrane potential across a selectively permeable nerve fiber membrane, as illustrated by the diffusion of potassium ions?
What is the approximate resting membrane potential of large nerve fibers when they are not transmitting signals?
What is the calculated Nernst potential for potassium ions in a normal nerve fiber, given the concentration gradient?
During the depolarization stage of an action potential, what event occurs?
What is the role of the inactivation gate of the voltage-gated sodium channel?
What is the primary contribution of the continuously acting electrogenic Na+-K+ pump to the resting membrane potential?
According to the All-or-Nothing Principle, what happens once an action potential has been elicited at any point on a normal nerve fiber?
What is the primary mechanism of saltatory conduction in myelinated nerve fibers?
What is the absolute refractory period in a nerve fiber?
How do local anesthetics such as procaine and tetracaine reduce membrane excitability?
What is the typical velocity of action potential conduction in large myelinated nerve fibers?
What is the primary reason for the plateau in the action potentials of some cells like heart muscle fibers?
What is the typical threshold for stimulation required to initiate an action potential in a large nerve fiber?
What is the primary role of impermeant negatively charged ions, such as anions of protein molecules, inside the nerve axon?
The Goldman equation is used to calculate the diffusion potential when the membrane is permeable to several different ions. What three factors does this potential depend on?
What is the approximate duration of the absolute refractory period for large myelinated nerve fibers?
What is the 'safety factor for propagation' of a nerve impulse?
In the context of the nerve membrane, what is the key difference in permeability between potassium and sodium ions at rest?
What causes the repolarization stage of the action potential?
What is the main advantage of saltatory conduction in terms of energy conservation?
What happens during the repolarization stage of an action potential in a nerve fiber?
The Nernst equation is used to calculate the diffusion potential that opposes the net diffusion of a particular ion. What determines the magnitude of this Nernst potential?
What is the phenomenon of 'overshoot' during a large nerve fiber's action potential?
What is the approximate voltage that causes the sudden conformational change in the activation gate of a sodium channel, leading to its opening?
What is an 'acute subthreshold potential'?
How does the permeability of the nerve membrane to sodium and potassium ions change at the onset of an action potential?
What is the primary characteristic of the voltage-gated potassium channel that contributes to repolarization?
According to the text, how many impulses can be transmitted by large nerve fibers before the concentration differences of sodium and potassium are reduced to a point that action potential conduction ceases?
What is the proposed mechanism by which a deficit of extracellular calcium ions increases nerve excitability?
In the context of nerve signal transmission, what initiates the positive-feedback cycle that opens the sodium channels?
How does an electrical current from a negatively charged metal electrode excite a nerve fiber?
What condition must be met for the inactivation gates of the sodium channels to reopen after an action potential?
In the voltage clamp experiments by Hodgkin and Huxley, what substance was used to block sodium channels?
What is the primary factor that makes the resting membrane potential of a neuron so close to the Nernst potential for potassium?
During an action potential, what is the cause of the after-hyperpolarization phase where the membrane becomes more negative than the resting potential?
What is the calculated membrane potential in a nerve fiber using the Goldman equation, considering only sodium and potassium diffusion with a K+ to Na+ permeability ratio of 100:1?
In the summary of events causing the action potential (Figure 5-10), what is the approximate ratio of sodium to potassium conductance during the early portion of the action potential?
What is the primary function of the nodes of Ranvier?
How much does sympathetic stimulation increase the activity of the Na+-K+ pump when intracellular sodium concentration rises from 10 to 20 mEq/L?
What is the 'electrochemical driving force' (Vdf) for an ion?
Which stage of the action potential is primarily responsible for signal transmission in neurons?
What is the primary method for measuring the membrane potential of a single nerve fiber?
The resting membrane potential is said to be 'polarized'. What does this term signify?
What are 'slow channels' in the context of action potentials in some cells like cardiac muscle?
If a nerve fiber membrane potential changes from -70 mV to -60 mV, but no action potential is fired, what is this potential change called?
What would be the effect on a nerve fiber of applying a positively charged electrode to its surface?
When does the inactivation gate of the voltage-gated sodium channel close relative to the activation gate opening?
What is the primary ionic event that terminates the plateau of a cardiac action potential?
How much does the permeability of the cardiac muscle membrane for potassium ions change immediately after the onset of the action potential?