Module 6: Neurons Flashcards

1
Q

What are some general facts about neurons?

A
  • They are the primary method of communication between the CNS and PNS.
  • There are about 100 billion neurons in the brain alone
  • Connections are determined by genes and other cues
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2
Q

What do dendrites do?

A

Receive chemical signals at their synapses

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3
Q

What do axons do?

A

Send electrical signals (APs)

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4
Q

What part of a neuron (besides dendrites) can receive electrical stimuli?

A

The cell body

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5
Q

What is membrane potential and RMP?

A

Membrane potential is the voltage across the cell membrane. RMP (Resting Membrane Potential) is the membrane potential when the cell is at rest.

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6
Q

Where is the normal RMP for a neuron?

A

About -70mV

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7
Q

What are the three factors which influence MP?

A
  • Difference in concentration gradients across the membrane for Na+ and K+
  • Difference in permeability of Na+ and K+
  • Electrogenic action of Na+/K+ pump
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8
Q

How does the difference in concentration gradients of Na+ and K+ determine MP?

A

Determines the electrochemical gradient and the extracellular fluid, and therefore the (degree of) ion movement

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9
Q

How does the difference in Na+ and K+ permeability affect MP?

A

Affects how much each ion will move in either direction

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10
Q

How does the electrogenic action of the Na+/K+ pump affect the MP?

A

It sets up the electrochemical gradients

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11
Q

What is the difference in permeability of Na+ and K+, and why does this difference exist?

A

There are many more non-gated ion channels for K+ than for Na+. Therefore, the resting permeability of K+:Na+ is 40:1

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12
Q

What does the Na+/K+ pump do?

A

It actively accumulates K+ in the cell, and forces Na+ out of the cell. This forms a high concentration of K+ inside the cell, and a high concentration of Na+ outside the cell.

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13
Q

Does RMP depend more on the Na+/K+ pump, or the non-gated ion channels?

A

Non-gated ion channels.

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14
Q

Why is the RMP so negative?

A

K+ is in a greater concentration and has greater permeability inside the cell. Therefore a lot of K+ leaks out, and each ion which leaves makes the cell interior one unit more negative. As K+ leaves on a large scale, and is not replaced by the introduction of more Na+, the overall effect is to make the RMP negative.

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15
Q

How do negatively charged proteins affect RMP?

A

They don’t as the cell is impermeable to them

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16
Q

How does Cl- affect the RMP?

A

It doesn’t, as Cl- doesn’t undergo active transport and so tends to sit at equilibrium.

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17
Q

What allows a membrane potential to be upheld?

A

The cell membrane’s ability to separate charge.

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18
Q

What is the patch clamp technique?

A

A method of measuring membrane potential.
It involves applying a pipette and small amount of suction to a cell membrane so that no ions can flow between the two. Therefore, when a single ion channels open, all ions must be released into the pipette. The current it generates can be measured with an amp connected to the pipette. This allows it to be known when the channel is open or closed, and the difference between the inside and outside of the cell.

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19
Q

What is a second method of measuring membrane potential?

A

Using a micro-electrode inserted into the cell, and recording cell voltage relative to a reference electrode.

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20
Q

What are the two equations which can be used to calculate MP?

A

The Nernst Equation

The Goldman Equation

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21
Q

What does the Nernst Equation measure?

A

It calculates the MP of cells where the membrane is only permeable to a single ion, so the RMP also depends on that single ion.

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22
Q

What is the Nernst equation’s formula?

A

E(ion) = 61.5mV x log([ion]o / [ion]i)
Where:
E(ion) = the equilibrium potential of the ion
[ion]o = the concentration of the ion outside the cell, and
[ion]i = the concentration of the ion inside the cell.
(These two can also be used as a ratio).

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23
Q

What is the assumption associated with the nernst equation?

A

Equilibrium is at body temperature

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24
Q

What are the limitations of the Nernst equation?

A

This does not account for permeability or ion conductance. It cannot accurately calculate the MP for a membrane permeable to more than 1 ion.

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25
Q

What are the positives of the Nernst equation?

A

No foreknowledge of permeability is required
It gives us the equilibrium voltage of a single ion (so what the voltage of a cell would be if it were only permeable to a single ion)

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26
Q

For what type of cells can the Nernst equation be used to calculate RMP?

A

Glia cells, as they rely only on [K+]

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27
Q

What does the goldman equation measure?

A

It measures the permeability and concentrations of multiple ions, allowing a representative RMP to be calculated.

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28
Q

What is the formula of the goldman equation?

A

Vm = 6.15mV x log ( (Pk[K+]o + Pna[Na+]o) / (Pk[K+]i + Pna[Na+]i) )
Where: P= permeability to
Vm = RMP

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29
Q

What is the effect of the cell membrane being more permeable to a certain ion?

A

RMP is shifted toward the more permeable ion’s own equilibrium potential.

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30
Q

What does membrane permeability mean for a comparison between neuron and glia cells’ RMPs?

A

As glia cells are only permeable to K+, their RMP is closer to K+’s eq. potential of -80mV than neurons are, as neurons also take into account Na+’s +60mV eq. potential.

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31
Q

What is an AP?

A

A brief fluctuation in membrane potential, caused by the transient opening of voltage-gated ion channels, spreading from there along the neuron.

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32
Q

What is the first step in the generation of an AP?

A

A stimulus causes the membrane to become more and more positive by changing the cell’s permeability to ions (especially Na+).

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33
Q

What are the different forms of stimulus?

A

Physical (light, current, stretch)

Chemical- drugs, synaptic excitation

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34
Q

What is the step in the generation of an AP involving a threshold?

A

Once the membrane has been depolarized to a point called threshold (approx. -55mV), a full on action potential is generated.

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35
Q

What happens after threshold is reached?

A

Voltage-gated Na+ channels suddenly open all at once, causing a great influx of Na+ and depolarizing the cell. This increases past 0mV, and the membrane potential becomes positive (called the overshoot)

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36
Q

Why do the Na+ channels open after threshold, and what are the processes which follow in the ion channels?

A

Their activation gates are voltage sensitive. Once threshold has been reached, the activation gates open, allowing Na+ to be very permeable (due to its electrochemical gradient). Their movement slows as the MP becomes more positive and attracts Na+ ions less. Then, the inactivation gates at the bottom of the channel close, preventing ions from flowing through. Once RMP is restored, the activation gates re-form

37
Q

How does a cell repolarize after threshold?

A

The Na+ channels inactivate and voltage-gated K+ channels are activated due to the positive potential. K+ floods the cell, making it more negative.

38
Q

What is hyperpolarisation?

A

The K+ gates are slow to close, making the MP slightly more negative than it was originally, until the cell returns to RMP.

39
Q

What is amplitude?

A

The difference between RMP and the peak of the overshoot

40
Q

What are absolute and relative refractory periods, and why are they important?

A

The absolute refractory period occurs during repolarization, and the relative refractory period is during hyperpolarization. It is important as when in these states the neuron cannot re-generate an AP, so their length determines the time between potentials for a neuron.

41
Q

How are APs simulated using a battery and piece of axon?

A

When the switch is activated, current flows from the cathode to anode. Most current travels across the membrane due to less resistence, but some moves inside the axon, and then back out into the anode, attracting positive ions as it goes. This causes local hyperpolarisation at the cathode and depolarisation at the anode. If voltage is large enough, depolarisation at the anode can reach threshold and generate an AP.

42
Q

Why is an AP generated due to the movement of current out of the axon?

A

When current flows from outside to inside the membrane, it causes hyperpolarisation, while as it flows from inside to outside the membrane, it causes depolarisation. This is because current is made up of electrons

43
Q

What is passive spread?

A

When an axon is stimulated, it becomes subthreshold, meets threshold and then fully depolarizes. Adjacent to the newly positive part are negative parts, which become attracted to the positive area and vice versa, causing some positive ions to move to the negative areas, slowly depolarizing them. If the depolarizing membrane reaches threshold too, the cycle repeats.

44
Q

Where does passive spread occur? What does this mean for the distance and speed the AP can travel?

A

Only in unmyelinated axons, and so involves the loss of much of the positive charge out of the membrane. As a result, the depolarization wave can only spread a short distance before fading, and transmission is very slow due to the necessity of having APs generated every step to sustain the depolarisation.
Therefore, passive spread can only occur in short or unimportant transmission. (smell).

45
Q

How have the characteristics of passive spread been proven?

A

Using a glass microelectrode to measure different MPs across the axon after generation of an AP. The depolarisation faded the further from the AP.

46
Q

What is saltatory conduction?

A

In myelinated axons, the myelin acts to insulate the axon and prevent current from leaving the axon until the next action potential is generated.
Therefore, axon potentials don’t need to be generated as frequently in the transmission as the current can travel longer distances without fading.
As a result, the axon only generates APs at the nodes of ranvier, where there are gaps in the myelin, and the current can dissipate out, causing another AP

47
Q

What is advantageous about saltatory conduction?

A

The time taken for the membrane to reach threshold is decreased, as charge remaining is more positive. Therefore, the myelin increases the distance an AP can travel

48
Q

What forms the myelin sheath on axons?

A

In the CNS it is formed by ogliodendrocytes.

In the PNS it is formed by schwann cells

49
Q

Why are unmyelinated axons still produced, if they take longer to pass information?

A

They are smaller, so more of them can be packed into a single area, allowing for more transmission networks, such as in the brain.

50
Q

What is the process of a stimulus acting on a sensory neuron? + example

A
  1. A graded depolarisation occurs in its sensory endings, know as the receptor potential. Its intensity depends on the intensity of the stimulus
  2. The receptor potential spreads passively to a trigger zone. If it meets threshold, an AP is generated.
  3. The AP is spread to the CNS, containing information about the strength of the stimulus and its frequency
    eg. a mechanical stimulus acting on a muscle spindle
51
Q

What is different about muscle cell’s channels when considering Receptor potential?

A

The muscle cell’s channels are cation specific, not ‘ion’ specific. Its amplitude depends on the stretch of the muscle, determining the number of APs generated in the trigger zone.

52
Q

What is synaptic transmission?

A

The process of transferring information from neuron to neuron or neuron to muscle fibre. It occurs very fast, by either chemical or electrical synapses (chemical most common)

53
Q

What is a neuromuscular junction?

A

The synapses between nerves and muscle fibres

54
Q

What is the general process of a chemical synapse?

A

An AP causes depolarisation in the presynaptic terminal, causes a neurotransmitter to be released, which diffuses across the synaptic cleft and binds to post-synaptic membrane receptors. This initiates opening of a channel in the post-synaptic membrane, causing or inhibiting an AP.

55
Q

What are the 3 important features of a chemical synapse?

A
  • Specificity: A neurotransmitter has a specific effect on the postsynaptic membrane
  • Complexity: the type, time course, strength and location of the synapse affect the response
  • Plasticity: changes in synaptic structure and function are associated with growth, development, ageing and learning.
56
Q

What are neurotransmitters?

A

Chemical messengers which open and close the cell membrane in order to depolarise or hyperpolarise the post synaptic membrane.
Each can bind to different types of receptor, and each produce a different effect with them.
This ability of diversity is critical for the range of human behaviours we have.

57
Q

What are the two types of chemical synapses in the CNS and PNS?

A
  • Excitatory synapses- depolarize the postsynaptic membrane by producing Excitatory postsynaptic potentials (EPSPs)
  • Inhibitory synapses- evoke hyperpolarisation of the post synaptic membranes via Inhibitory postsynaptic potentials (IPSPs)
58
Q

What neurotransmitters do excitatory synapses use, and how do they work?

A

They use Glutamic acid (glutamate) and ACh. They open cation specific channels in the postsynaptic membrane, depolarizing it closer to threshold

59
Q

What neurotransmitters to inhibitory synapses use?

A

GABA and glycine, and open Cl- or K+ channels.

60
Q

How does opening K+ channels inhibit APs?

A

More K+ is able to heave, causing the membrane to become more negative

61
Q

How does opening Cl- channels inhibit APs?

A

This decreases the resistance of the membrane, allowing any current travelling by passive spread to diffuse out of the axon more easily, making it less efficient for AP transmission and less likely that subsequent APs will be generated.
It does NOT affect membrane potential.

62
Q

What is the general process of an EPSP?

A

An AP causes depolarisation in the presynaptic terminal, opening Ca2+ channels. These ions flow into the presynaptic terminal and bind to vesicles of neurotransmitters, causing them to exit the membrane via exocytosis.
The neurotransmitters cross the synaptic cleft, binding to receptors in the post synaptic membrane.
They act as ligands in the ligand gated cation channels, allowing these channels to open and cations (esp. Na+) to enter the postsynaptic membrane, causing an AP.

63
Q

How do you make it more likely that an EPSP will generate an AP?

A

Use temporal or spatial summation

64
Q

What is spatial summation?

A

Threshold is reached due to multiple synapses on the same postsynaptic terminal produce EPSPs, leading to more stimulation than a single EPSP and increases likelihood of reaching threshold and generating an AP

65
Q

What is temporal summation?

A

EPSPs are produced by a single presynaptic membrane in quick succession. The MP does not have time to repolarize between synapses, so the MP gets higher and higher until threshold is reached.

66
Q

What are the two methods of gating ion channels?

A

Direct

Indirect

67
Q

What is direct gating?

A

It’s very fast, short lasting. The channel opens when the neurotransmitter binds

68
Q

What is indirect gating?

A

Occurs when a GPCR is activated by the neurotransmitter, activating a biochemical pathway by an enzyme binding to GDP and activating second messengers, like cAMP. This results in ion channels becoming phosphorylated, allowing them to open or close.
It’s slower and longer lasting than direct gating.

69
Q

What are some features and examples of small molecule transmitters (or classical neurotransmitters)

A
  • Fast
  • Work on direct gating
  • Eg. amino acids (glutamate, GABA, glycine)
  • Amines (Dopamine, norepinephrine, serotonin)
  • Small molecule transmitters (ATP, NO (not stored in the pre-s membrane)
  • ACh
70
Q

What are some features and examples of neuropeptides (neuromodulators)

A
  • Large
  • Work on indirect gating
  • Modulate the effects of other neurotransmitters
  • Slow, more diffuse action- not point to point, so can affect processes further afield- called volume transmission
  • Eg. enkephalin, substrate P, NPY
71
Q

Why is it necessary to remove neurotransmitters?

A
  • Allow the cell to recognize the next signal
72
Q

What are the three methods of neurotransmitter removal?

A
  • Diffusion. Happens to all. The neurotransmitter follows its conc. gradients back to the pre s membrane.
  • Enzymatic degradation- eg. ACh is removed by AChesterase
  • Re-uptake and recycling: most common. This removes the neurotransmitter to the pre-s terminals and astrocytes, or synaptic vesicles (uses two different transporters)
73
Q

What is glutamate and what does it bind to?

A
It's a small molecule neurotransmitter, which binds to four different types of receptor:
Three directly gated receptors
- AMPA
- NMDA
- Kainate
One indirectly gated receptor
- Metabolic Glutamate receptor
The response it generates depends on which receptor it activates
74
Q

What 3 factors determine synaptic action?

A
  • Type of neurotransmitter
  • Type of receptor activated in post synaptic membrane
  • Number of receptors activated in post synaptic membrane- this is determined by plasticity and allows long term promotion or depression.
75
Q

What is excitotoxicity and what causes it?

A

Excitotoxisity is caused by too much glutamate, leading to excessive activation of its 3 directly gated receptors. As some proteases (enzyme which breaks down proteins) are Ca2+ sensitive, the overwhelming influx of the ion can cause the cell to begin suicide (apoptosis), causing neuron damage. It is linked with stroke, epilepsy, and traumatic brain injury

76
Q

Why are temporal and spatial summation crucial?

A

Each neuron has approx. 10k synapses, some excitatory and some inhibitory. Each only produces a very small potential, which decay as they spread passively to the axon terminal. Therefore, many of them or many in quick succession are needed to make an impact.

77
Q

What does Na+/K+ pump do, overall?

A
  • Active transport
  • Relies on ATP
  • K+ in, NA+ out
  • Set up ion gradients
78
Q

What is the function of non-gated Na+ and K+ channels?

A
  • The RMP depends on their numbers.

- They allow the RMP to be negative due to the concentration gradient AND permeability of K+ ions

79
Q

What is the function of voltage gated Na+ and K+ channels?

A
  • Closed when no AP.
  • Na+ start to open as threshold is neared.
  • At threshold, mass opening and entry of Na+.
  • K+ channels detect this depolarisation and open
  • K+ leaves slowly, allowing re/hyper polarisation ans Na+ close
80
Q

What is the function of the K+ ligand gated channel?

A
  • Opens when (inhibitory) neurotransmitters bind in the post-synaptic membrane.
  • Hyperpolarises the cell, preventing AP
81
Q

What is the function of the cation ligand gated channel?

A
  • Permeable to any positive ion
  • Activated by neurotransmitters
  • Important for synaptic transmission
  • Important in sensory neurons (but gated by stretch, not ligands)
  • Depolarise the membrane to threshold to promote and AP
82
Q

What is the function of the Cl- ligand gated channel?

A
  • Decreases membrane resistance, preventing AP

- If at eq, there in no net Cl- movement

83
Q

What is the function of the Ca+ ligand gated channel?

A
  • Prevalent on pre-synaptic membrane
  • Catalyses exocytosis of neurotransmitters
  • Opened by depolarization of pre-synaptic membrane
84
Q

What must be remembered about the frequency of different channels?

A

Different parts of the cell membrane have different numbers of each channel

85
Q

How do dendrites send APs from/to axons?

A

Passively, although they have Na+ and K+ channels

86
Q

What is the effect of glia cells having no Na+ channels?

A
  • Don’t generate APs

- RMP = EK+

87
Q

What must be remembered about the Ek and Ena values?

A

They are not fixed- they are affected by the concentrations of their ions in and outside the cell- the given values are for a particular concentration ratio. If this changes, RMP changes. eg. if the conc. of K+ outside the cell increased, the RMP is more positive as less K+ wants to leave

88
Q

Compare and contrast receptor potentials with EPSPs/IPSPs

A
  • Both are graded, so aren’t all or none
  • RPs depend on the stimulus strength, while the PSPs depend on the number or frequency of synaptic transmissions
  • Both spread to the axon terminal passively, bus PSPs spread through dendrites and RPs through the muscle spindle.