Neurophysiology 1 Flashcards
Within the scope of the Goldman equation, what is the single most important thing that has to happen to generate an action potential?
PNa must increase. The permeability of Na+ increases by 1,000 times causing a massive depolarization event that generates an action potential.
Do changes in Kout or Kin have a larger effect on Ek and Vm?
Changes in Ko b/c Ko concentration is usually low and relative permeability high.
What is the difference between absolute and relative refractory periods?
- Absolute refractory period = when Na+ channels are inactivated and CANNOT be activated under any circumstances.
- Relative refractory period = when the membrane potential is hyperpolarized and K+ channels are open (i.e. K+ has an even higher permeability than usual). Harder to initiate action potential b/c voltage dependent K+ channels open, pulling Vm towards Ek.
Action potential generation is regulated by separate positive and negative feedback loops. Describe the two loops briefly.
- Positive feedback loop: As Na+ channels begin to let Na+ enter cell the membrane begins to depolarize, this feeds back positively resulting in further opening of VOLTAGE-DEPENDENT Na+ channels.
- Opening of K+ channels in response to depolarization, lets K+ out of the cell, eventually causing hyperpolarization of the membrane. Hyperpolarization leads to the closing of Voltage-dependent K+ channels via Negative Feedback.
What segment of each domain in voltage-gated ion channels detects changes in voltage?
What is the part of the voltage-gated ion channel that acts as the inactivating “ball”?
- The S4 segment of each domain (1-4) is the voltage sensor that detects changes of voltage during depolarization and hyperpolarization leading to opening and inactivating of the ion channel.
- Note: The Na+ voltage gated channel has a more sensitive S4 segment, therefore begins to open sooner than the K+ voltage gated channel
- The IFM loop on the interior of the cell b/t domains 3 & 4 is the inactivating “ball.”
- Long QT syndrome is an ion channel pathology seen mostly in cardiac muscle. Describe briefly.
- How is the Action Potential Shape different in cardiac muscle than in other parts of the body?
- How is Long QT syndrome a problem for dentists?
- Long QT syndrome is a mutation in K+ channels that causes a longer Relative Refractory Period.
- Due to K+ channels reduced conductance
- Re-polarization is weak and delayed
- Distorts rhythm b/c new AP kicks in before membrane is re-polarized (during relative refractory period), thus second AP can’t be generated. - Cardiac muscle AP shape is less of a sharp triangle. The graph climbs normally, but after a short, quick drop the re-polarization process platoes and then drops quickly again.
- When patients get nervous in a dental chair their heart rate quickens significantly. With Long QT syndrome this may cause sudden cardiac death.
- May have to knock patient out or conduct dental treatment in a hospital.
Can increased pressure depolarize membrane leading to an action potential?
Yes
What parts of dendrites changes size and shaped related to received signal strength and frequency?
Dendritic spines are plastic: change based upon input, can increase with learning.
Nissl Bodies are ribosomes for protein synthesis found in the Soma of neurons. What part of the soma will you not find them?
In the Axon hillock. Site of initial AP generation
Where in neural cells are graded potentials converted to action potentials? How is this possible?
In the axon hillock graded potentials are converted to action potentials. This is possible because there is an increased prevalence of Na+ channels in the hillock than elsewhere.
Axons are not only responsible for transporting Action Potentials, they are also responsible for transporting proteins and biological building blocks to the pre-synaptic terminal as well as taking waste back to the Soma. What role does Tau play in this process and what disease is associated with its disfunction?
-In what population is this problem often seen?
The tau protein plays an important role in loading materials onto microtubules to be transported along the axon.
- Hyperphosphorylation doesn’t allow tau to function properly leading to a buildup of waste at the pre-synaptic terminal.
- This dysfunction in tau is associated with alzheimers disease.
- Seen at an increased rate in football players and others that have received multiple concussions
What are glia (glial) cells?
They are nervous system support cells. Non-neural cells.
Briefly describe the role the following glial cells play in maintaining the neural system:
- Astrocytes
- Microglia
- Oligodendrocytes
- Schwann Cells
- Astrocytes: Communicate between neurons and blood vessels, can release transmitters into synaptic cleft (contribute to pain signals in mouth)
- Microglia: Immune cells of nervous system
- Oligodendrocytes: Wraps myelin around MULTIPLE axons in the CNS
- Schwann cells: Myelinate SINGLE axons in the PNS
Passive current flow won’t get you very and Active current flow is slow. What are the two problems that really limit efficient neural signal passage? How do Myelin sheaths fix these problems?
Axons are “Leaky Capacitors”
1) Their membranes are too thin. This amplifies the amount of charge around the membrane b/c of their natural affinity for each other. Therefore, in order to depolarize the cell & generate an action potential an enormous electrical input is required as well as increased time and current (=increased # of ion channels).
- Myelin sheaths thicken the membrane lessening the opposing charges thus making it easier to depolarize and generate and AP.
2) Leak channels allow too many K+ ions to flow out of the cells (messes with Na/K gradient). Requires Na/K pump to work harder and use up even MORE energy.
- Myelin sheaths block many of the Leak channels
- Myelin sheaths also speed up signal passage via saltatory conduction
What 3 factors affect the speed of neuronal impulses?
- Temp
- Axon thickness; Thicker = faster
- Myelin sheath. Sheath acts as a conductor.
How does saltatory conduction increase speed of signal impulses through axons?
Myelin sheaths cover up the majority of the axon. Voltage gated channels only active at the nodes of Ranvier every ~1mm. AP jumps b/t these nodes.
-Increases speed 100X (1 –> 100 m/s)
Myelin sheaths increase resistance across membrane 5,000X and decrease capacitance across membrane 50X. What does this mean?
- Increased RESISTANCE means that myelin resists the movements of ions across the membrane 5000X more than the axon membrane alone. VERY hard for ions to cross membrane. Greatly decreases loss of K+ ions via Leak channels.
- Decreased CAPACITANCE means that myelin seperates charges across the membrane. This makes it much faster and easier to charge the membrane. Thus, requiring fewer channels that are concentrated at the nodes of ranvier.
- Note: Active current flow at nodes and passive current w/in Myelin.
How does multiple sclerosis affect Myelin?
Multiple Sclerosis is an auto-immune disease where T-cells target Myelin and damage it. This impedes neural transmission.
