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Physiology and Pathophysiology I

Lectures 7/8: Resting Membrane Potential and

Action Potential

Instructor: Yue-Qiao (George) Huang

Dept of Pharmaceutical Sciences

School of Pharmacy

[email protected]

678 407 7371

Office 3033

Comparison

Surface Leaner

I previewed the reading before class.
I came to class.
I read the assigned text.
I reviewed my class notes.
I made index cards.
I rewrote my notes.
I highlighted the text.
I looked up information.
I asked a classmate or tutor to explain the material to me.

Deep Learner

I asked myself: “How does it work?” and “Why does it work this way?”
I drew my own flowcharts or diagrams.
I broke down complex processes step-by-step.
I wrote my own study questions.
I reorganized the class information.
I fit all the facts into a bigger picture.
I closed my notes and tested how much I remembered.
I asked myself: “How are individual steps connected?” and “Why are they connected?”
I asked myself: “How does this impact my life?” and “What does it tell me about my body?”

Questions to guide your study

How is a resting membrane potential developed?

How do(es) the movement of sodium and potassium ions develop their equilibrium potentials?

What is graded potential? How is it similar to or different from resting membrane potential or action potential?

What are the steps leading to the development of an action potential by a cell?

What is the all-or-none law of action potentials?

What is saltatory conduction?

Learning objectives

Explain how a resting membrane potential develops by the separation of charges across the plasma membrane.

Describe the effect of the sodium-potassium pump on membrane potential.

Describe how the movement of sodium and potassium ions develops their equilibrium potentials.

List the steps leading to the development of an action potential by a cell.

Explain how changes in plasma membrane permeability and in voltage-gated channels lead to an action potential.

Learning objectives

Define the all-or-none law of action potentials.

Define saltatory conduction and explain how myelination with nodes increases the speed of conduction of action potentials.

Describe how the sodium-potassium pump restores the concentration gradients of ions disrupted by action potentials.

Define contiguous conduction of an action potential.

Discuss the role of the refractory period in the one-way propagation of the action potential.

Direction of information flow

Membrane Potentials

Resting membrane potential
Constant membrane potential present in cells of nonexcitable and excitable tissues when they are at rest
Na+, K+, A-
Nerve and muscle cells
Excitable cells
Have ability to produce rapid, transient changes in their membrane potential when excited (action potentials)

Extracellular and intracellular Ion Concentrations

Ideas more important than numbers

Protein anions

Active Transport by Na-K-Pump

The ionic concentration gradients of Na+ and K+ are established and maintained by active transport via Na+-K+-pump.

Aka Na+-K+-ATPase

For every ATP hydrolysis, 3 Na+ are pumped out, 2 K+ are pumped in.

A few definitions and concepts

Cations and Anions
Cation: Positively charged ions, such as Ca++, Na+, K+
Anion: Negatively charged ions, such as Cl-
Chemical (concentration) gradient
Moves from higher concentration to lower concentration
Electrical gradient (electrical field)
Positives repel positives
Positives attract negatives

Chemical Driving Force

Chemical (concentration) gradient

Moves from higher concentration to lower concentration

The bigger the concentration ratio, the bigger the chemical driving force

Electrical Driving Force

Electrical gradient (electrical field)

Positives repel positives; negatives repel negatives;

Positives attract negatives.

Like charges repel; opposite charges attract each other.

As the charge difference gets bigger, the electrical driving force gets bigger.

Dynamic balance between the chemical and electrical forces while K+ leaks out.

Plasma membrane

ECF

Extracellular

ICF

Intracellular

Concentration

gradient for K+

Electrical

gradient for K+

EK+ = –90 mV

(A– = Large intracellular anionic proteins)

Plasma membrane

ECF

ICF

Concentration

gradient for Na+

Electrical

gradient for Na+

ENa+ = +60 mV

Plasma membrane

ECF

ICF

Relatively large net

diffusion of K+

outward establishes

an EK+ of –90 mV

No diffusion of A–

across membrane

Relatively small net

diffusion of Na+

inward neutralizes

some of the

potential created by

K+ alone

Resting membrane potential = –70 mV

(A– = Large intracellular anionic proteins)

The Na+-K+-pumps actively transport Na+ out of and K+ into the cell, keeping the Na+ concentration high in ECF and K+ concentration high in ICF.

Given the concentration gradients, K+ leaks out of cell. While K+ leaks out of cell, the protein anions cannot pass the membrane out and remains inside, so the inside is more negative.

The diffusion of K+ creates an electro-gradient that opposes the chemical force. The balance between the decreasing chemical force and increasing electrical force drives the membrane potential to its equilibrium potential (-90 mV). At the mean time, Na+ leaks into the cell, driving the membrane potential to Na+ equilibrium potential (+60 mV).

Because there are more K+ leak channels than Na+ leak channels, K+ exerts a stronger effect on the membrane potential. As a result, the resting membrane potential (-70 mV) is closer to -90 mV than to +60 mV.

Resting Membrane Potential:

3 key players

Figure 3.23: Counterbalance between passive Na+ and K+ leaks and the active Na+–K+ pump. At resting membrane potential, the passive leaks of Na+ and K+ down their electrochemical gradients are counterbalanced by the active Na+–K+ pump, so no net movement of Na+ and K+ takes place, and membrane potential remains constant.

Summary of RMP

All cells display membrane potentials, but only neurons and muscle cells (and some gland cells such as beta cells, adrenal chromaffin cells) are excitable.

Na+-K+ pumps establishes and maintains the Na and K concentration gradients.

At resting condition, leak K+ channels are open, allowing K+ to diffuses out of the cell. The diffusion of K+ creates an electro-gradient that opposes the chemical gradient.

When the electro-gradient is equal to the chemical gradient, the net flow of K+ is zero. Nernst equation. Equilibrium potentials.

The resting membrane potential results from mainly diffusion of K+, and to a lesser extent, diffusion of Na+.

Types of Changes in Membrane Potential

Membrane electrical states
Polarization
Any state when the membrane potential is other than 0 mV
Depolarization
Membrane becomes less polarized than at resting potential
Repolarization
Membrane returns to resting potential after having been depolarized
Hyperpolarization
Membrane becomes more polarized than at resting potential

Types of Changes in Membrane Potential

de- down, from (dehydration; dehumidify)
extra- outside of, in addition to, beyond
intra- within (intracellular: within cells)
hyper- excessive, above (hyperglycemia: high blood glucose level)
re- back, backwards, again (refurbish; retype; retrace; rewrite)

Medical Terminology: FYI

Neural Communication

Two kinds of potential change
Graded potentials
Serve as short-distance signals

Action potentials
Serve as long-distance signals

Ion movement

Electrical signals produced by ion movement across a membrane
Specific channel-mediated transport
Leak channels: open all the time
Gated channels: can open and close, regulating permeability
Voltage gated channels
Chemically (ligand) gated channels
Mechanically gated channels
Thermally gated channels

Graded Potentials

Local changes in membrane potential
Occur in varying grades or degrees of magnitude (strength).
-70mV to -60mV is a 10mV graded potential

The stronger the trigger, the larger the response - graded potential

Trigger will open an ion channel in a small, specialized region of the membrane
Usually vg Na+ channel

Graded Potential

Occurs in small, specialized region of excitable cell membranes
Magnitude of graded potential varies directly with the magnitude of the triggering event (stimulus)

Graded Potential

Magnitude of graded potential decreases as it travels in two directions locally

Summary: Graded Potentials

The stronger a triggering event, the larger the resultant graded potential
Graded Potential spread by passive current flow.
Graded potentials die over short distances
K+ leaks out of the membrane
Decremental: gradually decreases
If strong enough, graded potentials trigger action potentials

Action Potentials

Brief, rapid, large (100mV) changes in membrane potential: potential actually reverses

Involves only a small portion of the total excitable cell membrane

All-or-nothing

Conduction without decrement

Action Potentials

When membrane reaches threshold potential
Voltage-gated Na+ channels in the membrane undergo conformational changes

Flow of sodium ions into the ICF reverses the membrane potential from -70 mV to +30 mV

Flow of potassium ions into the ECF restores the membrane potential to the resting state

Three States of VG Na+ Channels (Ball and Chain Model)

Closed

Open

Inactivated

Action Potentials

Additional characteristics
Sodium channels open during depolarization by positive feedback.

When the sodium channels become inactive, the channels for potassium open. This repolarizes the membrane.

An action potential at one point in the plasma membrane regenerates an identical action potential at the next point in the membrane.

Therefore, it travels along the plasma membrane undiminished.

Action Potentials

Na+/K+ pumps gradually restores the concentration gradients disrupted by action potentials.

Sodium is pumped out of the cell
Potassium is pumped into the cell

Axon Hillock

Conduction of Action Potentials

Two types of propagation
Contiguous conduction
Conduction in unmyelinated fibers
Action potential spreads along every portion of the membrane

Saltatory conduction
Rapid conduction in myelinated fibers
Impulse jumps over sections of the fiber covered with insulating myelin (from node to node)

Contiguous Conduction

Saltatory Conduction

Propagates action potential faster than contiguous conduction
AP does not have to be regenerated at myelinated section
Myelinated fibers conduct impulses about 50 times faster than unmyelinated fibers of comparable size
Myelin
Primarily composed of lipids
Formed by oligodendrocytes in CNS
Formed by Schwann cells in PNS

Principles of Action Potentials

1. The All-or-Nothing Principle:

Action Potentials occur in all or none fashion depending on the strength of the stimulus

2. The Refractory Period:

Responsible for setting up limit on the frequency of Action Potentials

Refractory Periods

Absolute refractory period:
Membrane cannot produce another AP because Na+ channels are either open or inactivated

Relative refractory period occurs when VG K+ channels are open, making it harder to depolarize to threshold

7-38

Marieb Figure 11.13

Threshold

Action

potentials

Stimulus

Time (ms)

Coding for Stimulus Intensity

Summary of AP

Action potential is a fast depolarization, followed by repolarization back to the RMP. APs have three basic characteristics: stereotypical size and shape; propagation and all-or-none response.

AP either occurs or does not occur.

At threshold potential, fast opening of voltage-gated Na+ channels allow Na+ to flux into the cell, further depolarizing the membrane; and further depolarization activates more Na+ channels, providing a positive feed-forward loop for Na+ activation, rapidly raising the membrane potential to its peak.

Near the peak of AP, Na+ channels inactivate, and K+ channels open, allowing K+ to diffuse outside. This is responsible to the repolarization. For a brief period after repolarization, the membrane is driven closer to K equilibrium potential (hyperpolarization).

Summary of AP

Propagation of AP occurs by the spread of local currents from active regions to adjacent inactive regions.

Saltatory conduction of AP is made possible by the myelination of axons.

Contiguous conduction occurs when the axon is not myelinated.

The basis for the absolute refractory period is the inactivation of Na+ channels until the membrane returns to the resting membrane poptential.

The basis for the relative refractory period is the higher K+ conductance than is present at rest.

Increased intensity in stimulus causes more action potentials (that is, an increase in firing frequency), but has no effect on size/shape or travel speed of the APs.

Review Study Questions

What are cell bodies, dendrites, axons, and axon terminals?

What is a resting membrane potential?

What types of cells are “excitable”?

Can a graded potential be stronger or weaker? Can an action potential? Which one degrades over time?

How does a cell change its membrane potential? Be specific (what type of gates are used?)

Where does an AP start? What must happen here for an AP to be triggered?

Which channels open the fastest during an AP?

Which close first?

At the peak of an AP, is the Na+ channel locked, or can it be opened right away? What significance does this have to the neuron?

Review Study Questions

What is the rising phase of the AP called?

What is the falling phase called? What causes this? Do those channels lock?

When the falling phase over shoots resting potential, this is called what? Why does this happen?

How is “absolute” different from “relative” refractory period?

How does the refractory period cause conduction to be unidirectional?

What does “conduction without decrement” mean with regard to axons? “All or nothing”?

Do graded potential display the above properties? Why or why not?

Do all neurons have the same threshold? Do all have the same speed of conduction?

How does neuron diameter affect speed?

How does myelin affect conduction speed?