Synaptic Physiology III Flashcards
Do all cells have approximately the same ionic composition, and are they all bathed in extracellular fluids with approximately the same ionic composition?
yes and yes
What is the main determinant of the resting membrane potential of a cell?
Relative permeability to the different ions
Why is the following statement wrong? “Hyperkalemia (elevated potassium ion concentration in the blood) makes the extracellular fluid very positive with
potassium ions, which hyperpolarizes neurons.”
Extracellular fluid is always electrically neutral. Hyperkalemia must be accompanied by a decrease in other cations, or an increase in some anion (or both).
What is the effect of hyperkalemia on membrane potential of neurons? Why?
Depolarization. Hyperkalemia makes the concentration of potassium on the two sides of the membrane more nearly equal, which moves the potassium equilibrium potential towards zero. Because neurons are relatively highly permeable to potassium, the membrane potential follows, and the neuron depolarizes.
How does the activity of the sodium pump contribute to membrane potential in a big cell with relatively few ion channels? In a cerebral cortical neuron with long, thin
processes (i.e., large surface area) and many active ion channels (i.e., action potentials)?
In big, tight cells, the sodium pump plays only a long term role, and blocking it has little or no immediate effect on membrane potential. In small, leaky cells with high fluxes of sodium, the pump’s role is more immediate (these cells fill up with sodium and lose potassium quickly if the pump is blocked).
What is the function of APs?
To conduct electrical signals rapidly over long distances
What cell types give APs?
Neurons and muscle fibers
How are cells that give APs like cables?
They are cylindrical, and have a relatively low resistance interior that is covered by a insulator (the cell membrane), which is somewhat leaky, electrically speaking.
What is the typical length constant (lambda, λ) of a cell that can give APs?
about 1 mm, which means that an applied voltage will decay to about 1/3 (1/e) in one λ , ~1/9 in 2 λ , etc.
What is the function of the voltage-gated sodium channel in the AP?
It acts as a ‘booster station’, restoring the depolarization that would otherwise decay due to the leaky cable properties of the axon
What are the two key components of any ‘booster station’?
An energy supply (to boost the decaying signal) and a detector (to know when to apply the boost)
In a neuron, what is the energy source of the boost, and what is the detector?
The energy for the boost comes from the sodium ‘battery’ (the difference between the membrane
potential and ENa). The detector is the sodium channel activation gate (which is opened by the depolarization created by the approaching AP)
How is the rising phase of the AP like an explosion (an example of positive feedback)?
Depolarization → Activation gates open → Sodium enters → more depolarization → …
What is the role of the inactivation gate in
the sodium channel?
To make the channel stop conducting, even though the membrane is depolarized (i.e., the activation gate is still wide open)
What is the role of the voltage-gated
potassium channel in the AP?
It speeds up repolarization, shortening the duration of the AP.
What is the refractory period?
After giving an AP, an axon is less able to give another AP for a while
What is the mechanism of the refractory period?
Inactivation gates are still closed and potassium channels are still conducting immediately after the AP finishes.
How can a slow, steady depolarization (for
example, hyperkalemia) interfere with AP
generation?
The slow depolarization closes inactivation gates,
essentially knocking out those sodium channels
Define the safety factor for AP
propagation.
Axons possess more than the minimal number of sodium channels required for conduction.
What happens to the AP safety factor at an
axonal branch point? Why?
The safety factor is reduced, because the current produced by the membrane approaching the branch point is divided in two.
How does myelin work?
It wraps the axon membrane, reducing membrane leakiness and (by virtue of increasing membrane thickness) reducing capacitance.
Name several ways of increasing AP
conduction velocity in an axon
bigger diameter, less leaky surface membrane, higher density of sodium channels
What role does the sodium pump play in
the AP?
None. Eventually, though, it must pump out the
sodium and reabsorb the potassium ions.
How long does a nerve AP last?
about 1 ms
How long does a ventricular muscle AP
last?
about 250 ms
What are the 2 main channels that create
the cardiac AP plateau?
The ‘anomalous rectifier’ – this potassium channel closes with depolarization, and the voltage-gated
calcium channels provide inward movement of this
cation.
How long does a skeletal muscle AP last?
about 1 ms
When an axon is stimulated to threshold (away from its end), how many APs are created?
Two – they travel in opposite directions away from the stimulus site.
When an axon is stimulated at 2 sites, and 4 APs are created, what happens to the 2 APs that collide with each other? Why?
They obliterate each other, because behind each AP the membrane is refractory.
If the intracellular and extracellular fluids of an axon were switched, what would happen to the membrane potential? Could the axon give an AP? If so, would it be upside down?
The membrane potential would be positive (about +80 mV). This would close all inactvation gates, so it could not give an AP. (If in addition to switching solutions the membrane were inverted like a sock, then it could give an upside down AP).
An extracellular recording of APs from a nerve trunk is smaller than an intracellular recording of an AP from a single neuron. Why?
The extracellular recording measures the tiny currents flowing in the extracellular space, which produce a potential change of only a millivolt or so.
The amplitude of an extracellular recording of APs from a nerve trunk is not all-or-none, but is graded with stimulus strength. Why?
As the stimulus is turned up, more axons are recruited, giving a larger signal.
How do calcium ions affect the action potential?
Ca++ binds to fixed negative charges on the outside surface of axons. This increases the (very, very localized) electric field across the membrane (hyperpolarization), which stabilizes activation gates in sodium channels in the closed position.
What is the effect of reducing calcium ion concentration in the ECF?
Axons begin to fire APs spontaneously as Ca++ unbinds from surface charges, reducing the membrane electric field (depolarization), causing sodium channel activation gates to open.
