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A Intro to Neuro > Action Potentials > Flashcards

Action Potentials Flashcards

1
Q

What are action potentials?

A
  • A rapid increase then decrease in Vm
  • Also known as AP, spike, neural impulse
  • An ‘all-or-none’ event (i.e. action potentials from a given neuron are all the same)
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2
Q

Direction of AP on axon diagram

A
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3
Q

Why are action potentials needed?

A
  1. Axons are often long – neurons can be huge cells! (not all neurons need APs, but most do)
    giraffes: several meters
    blue whales: 25 m. from fluke to brain sauropod dinosaur: 40–50 m. from tail to brain
  2. Axoplasm is a poor conductor of electricity axoplasm is ~107 worse conductor of
    electricity than copper wire
    a 1m. long axon that is 1 μm in diameter has an electrical resistance equal to 1010 miles of 22 gauge copper wire (10 times the earth-Saturn distance)
  3. Axons are leaky and passive potentials don’t conduct very far
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4
Q

Leaky axons and conduction

A
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5
Q

The Action Potential and its Phases

A
  • If a neuron is only slightly depolarized, it may not initiate an action potential
  • For an action potential to start, the axon hillock must be sufficiently depolarized to reach ‘threshold’ (about -40 mV)
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6
Q

Diagram of AP phases

A
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7
Q

Initiating an action potential

A
  • AP threshold is about -40mV

How does a neuron get depolarized to reach the AP threshold?
1. Sensory input - physical energy leads to change in Vm (transduction) e.g. pressure from thumbtack opens Na+ channels (each sensory system has unique mechanisms)
2. Neurotransmitter from other neurons

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8
Q

Depolarization and firing rate

A
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9
Q

Information is coded in firing rate

A
  • Neurons in different parts of the brain respond to different sensory inputs, memories, emotions, etc.
  • Even within one area of the brain, different cells respond with greater or fewer action potentials to different inputs
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10
Q

How is an action potential generated?

A

Answer: three ion channels are involved

  1. Potassium channels that are open regardless of membrane potential (i.e. they always ‘leak’
  2. Voltage-gated sodium channels
  3. Voltage-gated potassium channel
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11
Q

What does ‘voltage-gated’ mean?

A

That a channel changes shape and the pore can pass ions only at certain membrane potentials (usually depolarizatoin)

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12
Q

Leakage K+ channels

A
  • K+ constantly leaks out of axons
  • Largely responsible for resting potential (membrane is 40x more permeable to K+ than Na+ at rest

Two things are always happening at the cell membrane
1. Na+/K+ pump
2. K+ leakage

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13
Q

Voltage-gated Na+ and K+ ion channels

A
  • These channels are located in axon membranes
  • There is a high concentration of voltage-gated Na and K channels at the axon hillock (spike initiation zone) and at gaps in myelination
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14
Q

Voltage-gated sodium channels

A
  • Membrane depolarization alters channel shape
  • Channels open when the membrane is depolarized
  • Positive feedback: more open NaV channels increases Vm, opening more channels, etc.
  • Vm rapidly increases –> rising phase
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15
Q

Opening and closing of NaV channels

A
  • Depolarization makes NaV channels open and then they automatically close

Depolarize the membrane and keep it depolarized for seconds
Three NaV channel examples:
* Channels open at slightly different times
* Na+ flows inward
* Channels automatically close after about 1 ms
* Channels stay closed even though membrane stays depolarized (like a screen door with a spring automatically closes)

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16
Q

The voltage-gated sodium channel has ___ states

A

3

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17
Q

What are the 3 states of the NaV channel?

A

Open, inactivated, and closed

A protein plug can block ion flow even when the channel is open i.e. ion flow can be blocked two ways:
1. channel is closed
2. channel is open but pore plugged (i.e. inactivated) 

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18
Q

Flow chart of three states of voltage-gated sodium channel

A
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19
Q

Voltage-gated KV channel

A
  • Kv channels are simply open or closed
  • After membrane depolarization, Kv channels open about 1 ms slower than Nav channels
  • Kv channels are called “delayed rectifiers”
  • The addition of open Kv channels to K+ leakage channels, makes Vm decrease rapidly
    ->falling phase
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20
Q

How do Kv and Nav channels differ after depolarization?

A

Kv channels open about 1ms slower than Nav channels

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21
Q

What are Kv channels called?

A

Delayed rectifyers

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22
Q

How does the addition of open Kv channels to K+ leakage channels affect Vm

A

It makes it decrease rapidly (falling phase)

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23
Q

What two factors determine ion flow?

A

Conductance and driving force

24
Q

How do conductance and driving force determine ion flow

A
25
Q

Action potential shape results from changes in Nav and Kv conductances

A
26
Q

When the AP starts, the Na+ conductance is ___ and the membrane moves towards the ___

A

High

Sodium equilibrium point

27
Q

Later, K+ conductance is high and the membrane moves towards the ___

A

Potassium equilibrium point

28
Q

Resting state of AP

A

Vm = -65 mV

  • Na+/K+ pump always running
  • K+ leakage channels always open
  • Vm is closer to EK than ENa because the membrane is much more permeable to K+
29
Q

Depolarization of AP

A

Vm = -65 to -40 mV

Initial depolarization occurs through:
- Sensory stimuli
- Neurotransmission

30
Q

Threshold of AP

A

Vm = -65 to -40 mV

  • Membrane depolarization increases the probability that Na+ channels will open (even below -40mV)
  • Greater depolarization from -65 to -40mV makes more channels open and more Na+ flows into neuron
  • If the depolarization exceeds -40mV, the inward flow of Na+ exceeds the outward K+ current from leakage and slow Kv opening. This is threshold - the essential trigger for an action potential
  • Above threshold, positive feedback rapidly accelerates Na+ current
31
Q

What happens if the depolarization exceeds -40mV?

A
  • The inward flow of Na+ exceeds the outward K+ current from leakage and slow Kv opening
  • This is threshold - the essential trigger for an action potential
32
Q

Rising phase

A

Vm above threshold and increasing to 40 mV

  • Voltage-gated Na+ channels (Nav) continue to activate
  • High sodium conductance (gNa&raquo_space; gK)
  • Sodium rapidly enters cell
  • Vm moves upward towards ENa (62mV)
  • Driving force on Na+ decreases
  • Driving force on K+ increases
33
Q

Overshoot

A

Vm peaks around +40 mV

As Vm gets closer and closer to ENa:
- Driving force on Na+ decreases
- NaV channels quickly inactivate
- KV channels continue to open after a delayed start (high gk)
- Vm never reaches ENa (62 mV) because there is always K+ leaving the neuron)
- Large driving force on K+

34
Q

Falling phase

A

Vm moves down toward Ek

  • NaV channels continue inactivating
  • Kv channels continue to open
  • Vm approaches Ek
  • Driving force on Na+ increases, but Na+ can’t cross the membrane because channels are inactivated
  • Driving force on K+ decreases
  • gK&raquo_space; gNa
35
Q

Undershoot and return to resting potential

A

Vm moves below -65 mV (closer to EK) then returns to -65mV

  • Vm dips below -65mV because there are Kv AND Kleak channels open
  • NaV channels are inactivated and then de-inactivate (ready to fire another AP)
  • Kv channels close and Vm increases back to -65mV
36
Q

Absolute refractory period

A
  • The majority of NaV channels are inactivated and cannot open
  • New action potential impossible
37
Q

Is a new action potential possible in the absolute refractory period?

A

NAUR

38
Q

Relative refractory period

A
  • A sufficient number of Nav channels are de-inactivated (ready to open), such that an action potential can occur if sufficient depolarization
  • Greater depolarizatoin than normal is required to reach threshold and produce AP
39
Q

Is a new AP possible in the relative refractory period?

A

Yes, but a greater depolarization than normal is required to reach threshold and produce AP

40
Q

Ion channel genes and neurological disease

A

Many types of neurological disorders can result from ion channel mutations that affect action potentials:
e.g. migraine, epilepsy, deafness, paralysis, ataxia (lack of muscle coordination)

41
Q

Episodic ataxia type 1

A

In a mouse model, a single stimulus leads to reverberant action potentials

42
Q

Rare Diseases based on Ion Channel Mutations

A
  • Generalized epilepsy with febrile seizures
  • Benign familial neonatal convulsion
  • Episodic ataxia
43
Q

Generalized epilepsy with febrile seizures

A
  • Seizures start in early childhood
  • Na+ channel mutations, slow Nav inactivation
  • Neurons are hyperexcitable
44
Q

Benign familial neonatal convulsion

A
  • Frequent brief seizures
  • K+ channel mutations, reduced K+ current in falling phase
  • Neurons are hyperexcitable
45
Q

Episodic ataxia

A
  • Episodes of poor coordination of movement and balance (ataxia)
  • Various K+ channel mutations impair AP repolarization
46
Q

Ion channel toxins

A
  • Tetrodatoxin (TTX)
  • Saxitoxin (STX)
47
Q

Tetrodatoxin (TTX)

A
  • Puffer fish (“fugu”) ovaries, liver, intestines (from ingested bacteria)
  • 23 people have died since 2000 in Japan from fugu consumption
  • x1200 more toxic than cyanide and no antidote
  • blocks Na+ channels and stops action potentials (1mg is lethal)
  • muscle paralysis -> asphyxiation
  • TTX is a useful tool for studying the role of Na+ channels
48
Q

TTX is a useful tool for studying the role of ___

A

Na+ channels

49
Q

Saxitoxin (STX)

A
  • People are poisoned by eating shell fish that have
    ingested dinoflaggelates (algae – red tide)
  • x100 more lethal than sarin nerve gas
  • 0.2 mg lethal in humans
  • CIA suicide pills
  • also blocks Na+ channels and action potential
50
Q

STX blocks ___ and ___

A

Na+ channels and action potentials

51
Q

Local anesthetics

A
  • Locally and transiently block APs
  • The first discovered was cocaine
  • Coca-cola was made from alcohol + cocaine from cocoa leaves
52
Q

Mechanism of local anesthetics

A
  • Most widely used now is lidocaine
  • Blocks Na+ channels that are open or inactivated (not closed/de-inactivated)
  • APs in small axons are most affected because their Na+ channels must open to assure AP propagation
  • Luckily for us, nerves responsible for pain have small axons
53
Q

Action potential propagation

A
  • To affect other neurons, the AP generated at the axon hillock must propagate to the axon terminal and synapse
  • The inflow of Na+ that happens in an AP will depolarize neighboring patches of membrane to threshold
  • Propagation only one way down axon because the soma-side of the axon is refractory
54
Q

Myelination

A
  • Larger axons conduct action potentials faster
  • Myelination also speeds propagation without size increase
  • Ion channels concentrated at nodes of Ranvier
  • Myelin helps current flow down axon by blocking leakage and lowering axial resistance
  • Nodes spaced such that Na+ influx quickly reaches next node and AP jumps node-to-node
  • Saltatory conduction (“to leap”)
55
Q

Multiple Sclerosis

A
  • Autoimmune attack on myelin degrades AP conduction
  • Age of onset: 20-40
  • Genetics:
    -women 3-4 times as likely as men
    -siblings 5%
    -identical twins 31%
  • Environmental factors – living closer to the geographic poles, low vitamin D, smoking
56
Q

Multiple sclerosis symptoms

A
  • Blurred vision is often the first symptom
  • Limb numbness or weakness
  • Electric shock sensations
  • Fatigue

A Intro to Neuro (7 decks)

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