1.11 PHYS - Electrophysiology of Neurons Flashcards
What is the role of the soma on a neuron?
All input from outside sources onto neuron is brought to the soma.
The soma sorts this input and decides what to do with it.
Input can be summated at the soma and, depending on amount of action potential delivered, may cause action potential or not.
The density of voltage-gated channels can vary in different parts of the neuron. What would a high density of channels mean regarding action potentials? Where is the highest density usually found? What does having a high density of channels in the dendrites of some neurons result in? What is the role of the density of voltage-gated Ca++ channels at the presynaptic terminal?
High density = higher likelihood of action potentials, or greater ease in creating one.
Highest density usually in trigger zone of initial segment at start of axon. (think about this one).
High density of channels in dendrites = provide stronger connections between dendrites and initial segment.
High density of Ca++ channels at presynaptic terminal helps facilitate synaptic transmission.
How does action potential travel? How does action potential travel in a cell vs. a cylinder?
AP propagates via local currents down an axon. (see image).
In a cell the AP would travel in various directions wherease in a cylinder it would propagate from one end to the other.
How does AP travel into muscle?
Transverse tubules open to exterior of muscle fiber in order to receive AP.
Transverse tubules run transverse to muscle fibers and AP is delivered to the muscle fibers.
In theory, what would happen to the amplitude of an AP as it moves down the axon? (think about what would happen to current injected at a point). What factors cause this? (this is review stuff).
The AP, or current, would decay.
Membrane resistance: resistance to moving charge movement across the membrane.
Membrane capacitance: storing charge across the membrane.
Internal resistance: resistance to flow down the tube.
What is the membrane length constant, what is it equal too? (this is some physics B.S. but just get the general idea, we all know how he loves his equations :-)).
Membrane length constant = decay over space.
Proportional to the square root of (membrane resistance (RM)/ internal resistance).
How can you increase the length constant? (remember length constant = square root (RM/IR)). (this is review).
Reduce internal resistance (make axon larger).
Increase membrane resistance (put myelin sheaths on).
The larger a nerve is the ______ the conduction velocity?
The smaller a nerve is the _____ the conduction velocity?
Faster.
Slower.
The membrane time constant (t) is: the time required to charge the membrane.
Membrane time constant = membrane resistance (RM) x membrane capacitance (CM).
In an effort to decrease the time it takes to charge the membrane (time constant), what must be done (regarding equation above)? How could you do this?
Need to decrease membrane capacitance.
Myelin sheaths both increase membrane resistance and decrease capacitance.
Increase membrane resistance is not ideal in this situation but is for the length constant. (harder to lose charge).
Decreasing capacitance by using myelin shealths is ideal in order to decrease the time constant. (easier to activate membrane).
What cells create myelin (PNS vs. CNS)?
PNS = Schwann cells.
CNS = oligodendrocytes.
When it comes to transmitting signals over a long distance there are a couple options: a massive sheath of myelin or/ and a massive number of voltage-gated Na+ channels spread down the fiber. This would be of hefty metabolic cost to our bodies, what is THE alternative?
Saltatory conduction.
Offers speed at a lower metabolic cost.
How is saltatory conduction carried out? (hint: what are the Nodes of Ranvier?).
Myelinated axon has stretches of myelin separated by regions of axon (Nodes of Ranvier).
These stretches of axon or Nodes of Ranvier, have high densities of voltage-gated Na+ channels.
Regarding the voltage-gated ion channels, what are the two gates present? What is the sequence of events during the creation of an action potential? What is the effect of hyperkalemia or hypokalemia on these gates?
Each has an activation and an inactivation gate.
- At rest: Activation gate closed, inactivation gate open.
- Action potential (depolarization): Activation gate opens. Na+ floods cell. Inactivation gate begins to slowly close.
- Repolarization: Inactivation gate closes. K+ begins leaving the cell.
- Repolarization further: K+ leaves cells, both gates close.
- Hyperpolarization: K+ leaves cell, inactivation gate opens.
In a state of hyperkalemia: hyperpolarization may never take place => inactivation gate may never open => AP may never take place.
In a state of hypokalemia: cell will be severely repolarized constantly and a normal AP may not be able to depolarize cell.
What is the difference between signals generated in sensory neurons vs. axons? (review).
Sensory neurons do not need to be repolarized in order to generate another AP, they can stay above threshold and keep firing.
Axons have to hyperpolarize and reset before firing another AP.
Be familiar with differences in action potential mechanisms between axons and mammalian central neurons. The various types of neurons and thresholds.
- In central neurons (specifically lumbar motor neurons) the Na+ current is not activated until 25 to 40 mV positive to rest.
- The somatic Na+ channels are not inactivated at rest and significant sodium channel inactivation does not occur until the soma is depolarized about 20 mV.
- These differences mean that the neuron can be held at a depolarized level, closer to threshold, and discharge action potentials repetitively.
- A fast, outward potassium current helps with repolarization.
- A calcium-sensitive postssium current creates a large afterhyperpolarization phase.
- The repolarizations and hyperpolarizations are important because they can be manipulated to determine firing frequency.
- Upstroke of the action potential is the same (voltage-activated Na+ channels).
