Exam 2 - Action Potential and Neuro Intro Flashcards

1
Q

Describe the propagation of an electrical signal by fast sodium channels?

A

A stimulus depolarizes a section of the cell that opens fast sodium channels. The singal travels both directions along the cell depolarizing the membrane and opening more sodium channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Descibe the how the propagation of a signal in repolarization occurs?

A

Fast Na+ channel close quickly and potassium channels open, repolarizing the cell in the same direction as the depolarization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of feedback is used during opening of Na+ channels during depolarization?

A

Positive feedback

Na+ opening causes depolarization and more Na+ channels to open.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What structure(s) allow communication between the brain and muscles?

A

Motor neurons and release of neurotransmitters at the neuromuscular junction (NMJ).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the nACh receptor/channel?

A

A protein at the NMJ that has 2 binding sites for acetylcholine (neurotransmitter). The inside of the protein is lined with negatively charged amino acids that repel negatively charged ions (positvely charged ion specific). The majority of the current is Na+ that starts the action potential. Small amount of K+ leaks out but is mitigated by Na+ influx. Ca+ also can come in and depolarize the cell, but is large and doesn’t come in as readily as Na+.

Nicotine can simulate Ach and causes tremors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe how nAch receptors can lead to depolarization of the cell?

A

2 Ach have to bind to open the negatively charged pore and allow the positive charge in (usually Na+). This sets off the fast Na+ channels the are next to the Ach receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why are NMJ inportant for us to know about?

A

This is where our paralytics work.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe mAch receptors and their function during hyperpolarization?

A

Found in the heart and mediates pumping by hyperpolarization. They are GPCRs and are activated by acetylcholine, the alpha subunit activates K+ channels which causes K+ to leave the cell making it more electronegative. This makes Vrm more negative (hyperpolarized) and makes it take longer to reach an action potential.

Named because they respond to a substance called muscarine.

In the heart, this process maintains HR and with vagal stimulation slows HR down even more.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are the AV and SA node innervated?

A

The left vagus nerve attaches to the AV and the right vagus nerve attaches to the SA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do antimuscarnics work? What effect do the have in the heart?

A

They antagonize mAch receptors, which prevents K+ channels from opening making Vrm more positive, leading to shorter time to fire an action potential and more BPM.

Ex: Atropine - blocks vagus activity in the HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe how physical pressure can turn a neuron on?

A

There are baroreceptors that sense pressure in cells. Increased pressure causes widening of pressure sensitive Na+ channels that leads to influx of Na+. If cell become positive enough, it will lead to an action potential that goes back to the brain/brainstem for processing.

More pressure = more Na+ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define threshold?

A

The charge that a stimulus must depolarize the cell to in order to fire an action potential.

Not all cell’s have same threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is sub-threshold?

A

A stimulus that does not overcome the cell’s threshold and will not fire an action potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What would an action potential look like for a weak stimulus that barely meets threshold?

A

There can be a delay in firing the action potential; slower firing of the action potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is supra-threshold?

A

A strong stimulus that depolarizes the cell well above threshold, leading to a faster action potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do action potentials in the heart differ from other action potentials?

A

The action potentials take longer and are sustained (plateau) to allow effective pumping. This is due to slow Ca++ channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the role of Cl- in the nervous system?

A

Permeability is adjusted to hyperpolarize or supress excitable cells. This occurs via GABA receptors that open chloride channels in neurons; prevents overactivity like seizures.

“Brakes” of the nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe calcium’s role in action potentials?

A

Calcium is large, has double positive charge, and huge concentration gradient. So, it sits near the cell wall and will block Na+ leak channels, blunting cell electrial activity.

Results in a “calming effect”, by stabilizing membrane potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What effects would hypocalcemia have on the cells membrane potential?

A

Hypocalcemia results in an increase in Na+ influx through Na+ leak channels (because less Ca ions are blocking the channel). This makes the cell less polar and makes the membrane potential more positive (more excitable).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to membrane potential during hyperkalemia? How can this be corrected?

A

K+ will not leave the cell as much leading to a more positive membrane potential.
Giving Ca++ will block Na+ leak channels make the cell less positive, opposing the effects of hyperkalemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Wy doesn’t Ca++ also block K+ leak channels?

A

Because K+ is leaving the cell, so Ca++ will just be moved out of the way.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What effect does hypocalcemia have on motor neurons? What clinical sign does this cause?

A

Leads to a more positive resting potential and will cause hyperactivity of the motor neuron, leading to tetany.

Trusseau sign and Chvostek sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What other compound can aid in reducing cell hyperactivity (increased membrane potential)?

A

Mg++ helps to hyperpolarize the cell; provides similar effects to Ca++, but mechanism is not clear.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What effects the rate of electrial propagation in nerve fibers?

A
  1. Length of the nerve (longer nerve takes more time for signal to reach destination)
  2. Diameter of the nerve (Wider = Faster; less resistance)
  3. Insulation (myelin sheath = faster)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where can myelin be derived from?

A

The sphingomyelin in the cell wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What cell is involved in myelination in the periphery? How does it work?

A

Schwann cells. They wrap around the nerve in layers and as it does, all of the water is pushed out of the cell leaving a lipid compound that provides protection, speed, and efficency for neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is an action potential spread?

A

Through opening of fast Na+ channels. Na+ channels open causing depolarization that cause more Na+ channels to open.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the effects of myelination of nerve fibers?

A
  1. Speeds up rate of signal by blocking Na+/K+ pumps, preventing loss of Na+ and continuation of the signal.
  2. Reduces cell energy requirements because Na+/K+ pumps are not running as much. Less prone to ischemia.
  3. Protection from injuries or other forces.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the openings in between myleinated nerve fibers called?

A

Nodes of Ranvier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is important about the nodes of ranvier?

A

There is a high density of fast Na+ channels that help ensure the continuation of the signal to the next myleinated nerve fiber. (saltatory conduction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is one difference between myelinated and unmyelinated neurons?

A

Unmyelinated neurons have much more fast Na+ channels along them than unmyelinated neurons.

Although they may not have more overall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Why would a myelinated nerve fiber require MORE local anesthetic to block than and unmyelinated nerve?

A

Because of the high density of fast Na+ channels at the nodes of ranvier.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is saltatory conduction?

A

The “jumping” of an action potential from one node of ranvier to the next, due to Na+ being prevented from leaving the cell under the myelinated sections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What cells preserve and maintain myelin in the CNS?

A

Oligodendrocytes

These cells are not good at replacing lost myelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What cells preserve and maintain myelin in the PNS?

A

Schwann cells

Are able to replace some lost myelin much better than oligodendrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe what happens with demyelinating diseases?

A

When myelin is present the channels underneath the myelin will disappear beacuse they are not being used. When the myelin degrades, the Na+ and K+ channels are not replenished but, the Na/K/ATP pump is. So, during an action potential the Na channels are still far apart and the Na/K pump is in between pumping all of the Na back out, leading to inhibition of the signal which can result in paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some demyelinating diseases and their causes?

A

MS, Optic Neuritis, Guillain-Barre Syndrome
Causes: Genetics, infection, autoimmune hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are gap junctions?

A

Gap junctions are small pores/channels that allow movement of small ions (mainly Na+) from one cell to a neighboring cell (both forwards and backwards). This is used in rapid transduction of an electrical signal. The more gap junctions, the faster the signal is moved from one cell to the next.

The bidirectionality can be bad in the heart when a rogue electrical current can be allowed to move easily though gap juntions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the structure of a gap junction?

A

Comprised of 6 connexin proteins that make up a single connexon. 2 connexons lined up together make up the gap junction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the postsynaptic and presynaptic terminals?

A

Presynaptic is the sending cell. Postsynaptic is the recieving cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the myelination classifications?

A

A: Myelinated
B: Lightly myelinated
C: Non-myelinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does importance of a signal relate to nerve size?

A

The more important signals (motor functions) are sent through bigger, myelinated, neurons. Not so important signals are sent through smaller, unmyelinated neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the categories of A fibers? How are they classifed?

A

Alpha, beta, gamma, and delta. Classifed by size from largest to smallest.

44
Q

What is the soma?

A

The cell body of a neuron where the nucleus and lots of mitochondria are.

45
Q

What is the recieving structure in a neuron?

A

Dendrites

46
Q

Describe the membrane potentials in the excitatory portions of a neuron?

A

The dendrites have a more positve membrane potential than the rest of the cell that allows them to respond quickly to excitatory stimuli.

47
Q

Describe the membrane potentials in the inhibitory portions of a neuron?

A

The membrane potentials are more negative the rest of the cell.

48
Q

Describe the sending portion of a neuron?

A

The axon, most are myelinated but not at the presynaptic terminal so that neurotransmitters can be released.

49
Q

Describe the properties of the axon hillock?

A

The axon hillock is at the begining of the axon that is composed of inhibitory connections that suppresses the activity of the CNS via GABA.

50
Q

Describe how inhibition is accomplished at the axon hillock?

A

The hillock is comprised of inhibitory synapses that release GABA. GABA is the major inhibitory neurotransmitter and causes an incresase in Cl- permeability which results in hyperpolarization (inhibition/suppression).

51
Q

Describe the relationship between alcohol and GABA?

A

EtOH is GABA receptor agonist, which causes low production of endogenous GABA. When EtOH is taken away, there is not enough GABA to inhibit the nervous system leading to seizures.

52
Q

What are macro glial cells?

A

Astrocytes, ependymal cells, and oligodenrocytes.

53
Q

What is the role of astrocytes?

A

Important in the BBB by wrapping around the capillaries in the brain. They help maintain electrolyte and pH balance in the CSF.

54
Q

What is the role of ependymal cells?

A

They produce CSF and have cillia to move the CSF around.

55
Q

What is the role of microglia?

A

Digest debris that is within the CSF.

56
Q

Describe a multipolar nueron?

A

They are decision making cells. Decide wheter to fire AP or not. (Motor neuron)

57
Q

Describe a bipolar neuron?

A

Used in special organs for specialized senses. (Photoreceptors in retina and optic nerve).

58
Q

Describe a pseudounipolar neuron?

A

Majority of sensory function. Primarily just passing of information. Doesn’t need to make decisions.

59
Q

What does the term somatic mean?

A

Conciously sensible

60
Q

What are the function of free nerve endings?

A

Sensing and sending pain signals.

Also called nociceptors.

61
Q

Describe the adaptability of baroreceptors?

A

They will reset (adapt) themselves after exposure to a prolonged stimulus (elevated blood pressure). This gives the body the ability to respond to new changes. If they didn’t adapt, they would reach their limit for signal transduction.

62
Q

Why is fast adaption important?

A

Because the body cares more about new changes as opposed to staying focused on the one change. That way the nervous system is not overwhelmed with continual signaling.

63
Q

How many connections can a neuron have?

A

Some have 10,000+

64
Q

What is reverse adaptation? Where does this happen?

A

Is when cells do not reset or adapt to stimulus but become more sensitized instead. This happens with nociceptors. More pain = more sensitivity to pain.

65
Q

How can reverse adaptaion be managed?

A

Giving pain medication before the pain starts or by performing a nerve block. Once pain level is high it can be very hard to impossible to bring back down.

66
Q

How does a neuron propigate an action potential?

A

There are fast Na+ channels along the neuron that depolarize as the action potential moves down toward the synapse. There are VG K+ channels and Na+/K+ pumps also down the neuron to repolarize the cell. Once the neuron is depolarized to the terminal end, p-type Ca++ channels open which cause VP-2 vesicles to fuse with the membrane and release their contents.

67
Q

How are vesicles stimulated to release their neurotransmitter in a motor neuron? Explain the two types of vesicles in the neuron.

A

The action potential reaches the end of the neuron and open p-type calcium channels that allow Ca++ ions in. The Ca++ ions destabilze VP-2 storage vesicles that are close to the cell wall and cause them to empty ACh into the synapse.
The VP-1 vesicles are futher away from the wall and are not ready to be activated.

68
Q

What processes reset the cell in a motor neuron?

A
  1. The Ca++ ATP pump
  2. Na+/K+ pump
  3. VG K+ channels
  4. Ca++ sensitive K+ channels
69
Q

Describe end plate potential?

A

The initial depolarazation caused by opening of nACh-R of the recieving cell at a synapse. In a healthy muscle, these will always turn into an action potential because of fast Na+ channels next to the nACh-R.
This is possible because of the vast excess in number of receptors and neurotransmitters.

70
Q

How would our HR be affected if we did not have inhibition from mACh receptors?

A

Our heart would beat at about 120 bpm if there was no inhibition.

71
Q

What is the largest compartment in non-obese people?

A

The skeletal muscles

72
Q

What muscle cells are innervated by more than 1 motor neuron?

A

Occular muscles

73
Q

How many muscle cells does one neuron innervate?

A

Typically one cell, except for occular muscle

74
Q

What are the 2 ways a motor neuron can be activated?

A
  1. By the descending spinal tracts from the brain
  2. By the reflex archs
75
Q

What are the contractile elements in muscle fibers?

A

Actin and myosin, they cause the muscle fibers to shorten which results in contraction

76
Q

What is the specialized version of the endoplasmic reticulum found in skeletal muscle? What is its purpose?

A

Sarcoplasmic reticulum
Primary source of calcium for muscle contraction

77
Q

Describe the length of muscle fibers?

A

They are usually very long, some are 1 foot in length.

78
Q

What is the function of transverse tubules?

A

Crosses the muscle fibers transversely allowing the action potential to travel deep into the tissue via fast Na+ channels and DHP receptors.

79
Q

Describe the location of mitochondria in a motor unit and neuron?

A

There are lots of mitochondria situated close to the clefts of the postsynaptic terminal. They are also inside of the presynaptic terminal of the motor neuron.

80
Q

What are the names of the indicated structures?

A

Primary clefts and secondary clefts

81
Q

Describe the location of ACh receptors and fast Na+ channels in the NMJ?

A

Acetylcholine receptors are situated near the top of the clefts and the VG Na+ channels are towards the bottom of cleft as well as spanning the length of the muscle fiber.

82
Q

Where is acetylchoninesterase found? How does it break down ACh?

A

Acetylcholinesterase is attached to the skeletal muscle cell
It uses hydrolysis to break down an ester bond on ACh into Acetyl (acetate) and choline

83
Q

What type of macromolecule is acetyl or acetate?

A

Starch

84
Q

Where are schwann cell bodies located on a motor neuron?

A

They are situated near the end of the presynaptic terminal

85
Q

How many ACh receptors are present at the NMJ? How many are activated per action potential? How much Ach is released?

A
  • 5 million ACh receptors
  • 500,000 activated per AP (10 % of receptors)
  • 1 million ACh molecules minimum (each receptor needs 2 ACh), usually 2 million are released (some are destroed by acetylcholinesterase before reaching receptor)
86
Q

Why doesnt much K+ leave through the ACh receptor during activation?

A

There is a lot of Na+ and Ca++ flooding in and there are lots of K+ leak channels that K+ can leave through instead

87
Q

What organic compound can block ACh receptors? What drugs are modeled after it? How do they work?

A
  • Curare
  • NDMR
  • They block ACh from binding to the receptor, preventing depolarization (only one site has to be blocked to inactivated the receptor)
88
Q

How does the skeletal muscle detect an AP at the NMJ? How does lead to contraction?

A

Through DHP (dihydropyradine) receptors that are situated at the NMJ and transverse tubules. The receptors are tethered directly to Ca++ channels of the SR. They open these Ca++ channels when stimulated by an AP.

89
Q

What is the appearance of the DHP receptor? Can anything enter through them?

A

It looks like a VG Ca++ channel and a small amount of Ca++ does enter through them when activated.

90
Q

What are the names of the channels that DHP receptors open on the SR?

A

Ca++ release channel or RyR (ryanodine receptors)

91
Q

How is calcium put back into the SR after a contraction?

A

By the SERCA (Sacroplasmic Endoplasmic Reticulum Calcium ATPase)
This pump needs to use energy to move Ca against its concentration gradient (lots of Ca in the SR)

92
Q

Describe the E-C coupling pathway in skeletal muscle?

A
  • Motor neuron depolarizes due to AP sent by reflex arch or brain
  • Ca++ influx into MN by p-type Ca++ channels
  • ACh vesicles fuse to presynaptic terminal
  • ACh released into NMJ and binds to nACh receptors
  • Na+ and some Ca+ influx generates end plate potential (EPP)
  • EPP local depolarization leads to an AP
  • AP spreads lenghtwise down muscle fibers via fast Na+ channels
  • AP sensed by DHP receptors which cause release from RyR
  • Ca++ influx into sarcoplasm
  • Ca++ tucked back into SR by SERCA
93
Q

How is choline transported back into the neuron for recycling?

A

Choline ATPase and Choline Na+ transporter

94
Q

What is mitochodrias function in the neuron?

A

Source of ATP
Storage of acetate for ACh production

95
Q

Where can extra choline be found in the neuron?

A

In the cell membrane from phosphatidylcholine

96
Q

Describe myaesthenia gravis and how it affects the NMJ?

A
  • A person’s body makes antibodies against nACh-R (because of a faulty thymus)
  • The antibodies sit on the receptors triggering the immune system to destroy them
  • This causes scare tissue on the clefts reducing the amount of surface area for nACh receptors and fast Na+ channels
  • This leads to the inability to propagate an AP and progressive muscle weakness

Disease usually gets worse throughout day

97
Q

What are the treatments for MG?

A

Thymus removal, plasmapheresis, acetylcholinesterase inhibitors (-stigmines)

98
Q

Describe LEMS/ELMS and how it effects the NMJ?

A

Lambert-Eaton Myaesthenic Syndrome
*Oncology patients (usually lung) create antibodies against p-type calcium channels
*Results in Ca++ defeciency in MN which does not allow ACh to be released by vesicles

99
Q

What are the treatments for LEMS/ELMS?

A
  • AChesterase inhibitors will not work - Ach is not being released
  • Plasmaphereisis
  • Removal of lung tumors
  • K+ channel blockers (TEA - tetraethylammonium, 4,5-dihydropyradine) - these work by slowing repolarization which should allow more Ca++ in and cause ACh release
100
Q

Why are K+ channel blockers for LEMS/ELMS so dangerous?

A

They are not specific to only motor neuron K+ channels, they can effect channels all over body including the heart leading to cardiotoxicity

101
Q

Why is amiodoarone a safe K+ channel blocker?

A

Because it is not very specific for K+ channels, making it safer

102
Q

How do NDMR work?

A

They are nACh receptor antagonists, preventing ACh from binding and thereby preventing depolarization and muscle contraction.

103
Q

What is the main DMR and how does it work? What is its structure?

A
  • Succinylcholine
  • Its structure is 2 acetylcholines attached to each other
  • Causes sustained depolarization at nACh receptors which prevents reseting of local fast Na+ channels (an AP cannot be generated at NMJ)
  • AChesterase is not effective at breaking down succinylcholine
104
Q

What will you see when succinylcholine is first adminstered and why?

A
  • Fasiculations or twitching
  • Due to inital depolarization caused by activation of nACh receptors
105
Q

Describe the membrane potential change and its effects with succinylcholine administration?

A
  • The membrane potential in the skeletal muscle is much more positive due to all of the Na+ influx through nACh receptors
  • This causes K+ to be pushed out of the cell
  • This normally leads to a 0.5 mOsm increase in serum K+
106
Q

How do deinnervating diseases or strokes lead to worse hyperkalemia with succinylcholine than normal?

A

In muscle that has not been used much, they usually have additional nACh receptors away from the NMJ. This leads to more muscle fibers being depolarized than just at the NMJ. This leads to a more profound exiting of K+ and worseing hyperkalemia.