Nerve and synapses Flashcards

1
Q

What are the 3 types of fibers present in the PNS? Describe what they are.

A

Afferent (sensory): brings signals in and towards the CNS
Efferent (motor): sends signals from CNS to skeletal muscles
Autonomic: sends signals from CNS to visceral muscles

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2
Q

The smallest unit in the nervous system is the […]

A

neurons

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3
Q

What are synapses?

A

They are specialized sites where communication between neurons takes place.

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4
Q

Describe the standard structure of a neuron.

A

All neurons have a cell body, several branching dendrites and a single axon that can vary in length that ends in a presynaptic terminal

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5
Q

Describe the soma of the neuron.

A

This is where the nucleus and organelles, such as the mitochondria, are. It is also where chemical reactions and processes take place. It could survive if you removed all other parts of the cell.

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6
Q

Describe the dendrites of the neuron.

A

They allow neurons to receive inputs from other cells and are highly branched to allow more synapses from which they can receive signal

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7
Q

Describe the axon of the neuron.

A

A neuron only has one axon, which allows it to send information to other neurons using an electrical impulse that propagates to the presynaptic terminal.

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8
Q

Describe the flow of information in the neuron.

A

It comes in through the dendrites, travels into the soma, then travels down the axon towards the dendrites of another neuron.

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9
Q

What is the resting membrane potential of the neuron? What is the cause?

A

Around -70 mV compared to the outside. This is due to a small excess of negatively charged ions inside the cell.

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10
Q

Explain the two major causes of the voltage gradient in the neuron.

A
  1. There is a concentration gradient of Na+ (a lot on the outside, little on the inside), K+ (a lot on the inside, little on the outside), Cl- (a lot on the outside, little on the inside), and other anions (a lot on the inside, little on the outside).
  2. At rest, the neuronal membrane is only highly permeable to K+, which wants to flow out of the cell. So K+ will naturally leak out of the cell from leak channels down their concentration gradient, leaving behind unpaired negative ions that pull K+ back in.
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11
Q

Explain why the resting potential is a bit more positive than the Equilibrium of K.

A

While the K ions are trying to reach their equilibrium, there is a minuscule amount of Na that leaks into the cell (the membrane is not perfectly permeable) Because neither the Na nor K. ions reach their concentration gradients, if it was left to itself, the leaking would continue until there was no more concentration gradient. That’s why the Na/K pump is useful.

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12
Q

What does the K/Na pump do?

A

At rest, because there is a constant leaking of K and Na ions, the pump will be there to create and maintain the concentration gradient. It becomes the source of energy for the ions to keep moving.

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13
Q

When the neuron is at rest, the dominant ion determining the membrane potential is […]

A

K+

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14
Q

What are action potentials?

A

They are brief electrical impulses that axons propagate from one region of the nervous system to another.

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15
Q

Action potentials travel from the […] to the […] of a neuron

A

Initial segment, presynaptic terminals

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16
Q

What is the difference between depolarization and hyperpolarization?

A

Depolarization is when the membrane gets more positive
Hyperpolarization is when the membrane gets more negative

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17
Q

The action potential involves a [depolarization/hyperpolarization] from […] mV to […] mV

A

depolarization, -70 mV, the required

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18
Q

Explain the threshold potential and how it relates to the action potential.

A

electrical impulses are often sent but don’t always produce an action potential. It only produces an action potential if it’s above the threshold potential. If not, the membrane relaxes back to -70 mV without sending a signal.

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19
Q

The depolarizing phase of the action potential is caused by […]. Explain their critical 3 properties.

A

Sodium ions flowing into the cell through voltage-gated sodium channels. Sodium channels are (1) closed at resting membrane potential but open when the membrane depolarizes, (2) selective for Na+, (3) able to rapidly inactivate after opening, stopping the flow of Na+ ions.

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20
Q

Explain the process by which reaching the threshold of depolarization releases the action potential.

A

When the membrane depolarizes to it’s action potential threshold, a small number of Na+ channels will open and allow Na+ to flow in, further depolarizing the membrane potential. This will cause more Na+ channels to open, allowing more Na+ in and further depolarizing the membrane potential. This leads to a positive feedback loop at results in the membrane potential reaching +30 mV, closer to the Na equilibrium.

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21
Q

Why do action potentials top out at +30 mV?

A
  • The Na+ channels that open due to membrane depolarization quickly deactivate.
  • Some Na+ can still leak out. When the channels deactivate, there’s no more Na+ permeability, and the membrane potential returns to -70 mV.
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22
Q

Explain why Na+ is able to become the dominant ion when the membrane is depolarized.

A

The density of voltage-gated sodium channels in the axon membrane is much higher than the density of leak potassium channels, so at the peak action potential, Na+ permeability becomes much higher than the resting permeability for K+.

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23
Q

Explain the role of voltage-gated potassium channels in the action potential. What are they activated by?

A

Voltage-gated K+ ion channels are slowly opened when the cell membrane depolarizes. However, It is only really effective once the cell has started repolarizing. When those ion channels are open, it lets K+ out of the cell more than the leaking channels. This is to get the cell back to its resting potential faster [get more info to go through after]

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24
Q

What is the advantage of a short action potential?

A

Neurons send different messages with frequency and patterns. By having a short action potential, more information can be sent in a given period.

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25
Q

Explain how action potential propagation down the axon occurs.

A

The Na+ coming into the cell at the initial segment is going to be “attracted” by the other negative ions down the axon, and so the process of propagation is going to continuously regenerate all the way to the presynaptic terminal.

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26
Q

Why does propagation occur in one direction down the axon?

A

The Na+ voltage-gated channels are inactivated and is in a period of absolute refraction meaning that nothing will be able to open them in that period.

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27
Q

What are the absolute and relative refractory periods?

A

Absolute: The sodium channels are INACTIVATED, and so the membrane is completely unexcitable
Relative: The sodium channels are CLOSED while he voltage-gated potassium channels are open. The membrane potential is more negative than it’s resting potential meaning that the axon is less excitable than normal (you would need a bigger signal to activate it again)

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28
Q

How do neurons transmit specific information using action potentials?

A

with different frequencies and patterns

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29
Q

Neurotoxins are usually target […] in victims, because […]

A

sodium channels
They are important for all functions of the body

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30
Q

Puffer fish make the neurotoxin […]. Describe the effect that it has.

A

tetrodotoxin
It inhibits the opening of sodium channels. This means that the functions will be reduced if not everything is touched but could eventually lead to death (diaphragm paralysis)

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31
Q

Phyllobates frogs secrete the neurotoxin […]. Describe the effect that it has.

A

Batrachotoxin
It activates the sodium channels. This means that they always stay open and this big storm of action potentials causes seizures.

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32
Q

What types of drugs can block sodium channels?

A

Local anesthetics and antiepileptic

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33
Q

Give 4 examples of local anaesthetics that can block sodium channels.

A

Lidocaine
Benzocaine
Tetracaine
Cocaine

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34
Q

Give 2 examples of antiepileptics that can block sodium channels.

A

Phenytoin
Carbamazepine

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35
Q

What is the purpose of drugs that block sodium channels?

A

Local anesthetics will block any pain signal from getting to the brain (getting processed), while antiepileptic drugs will block the excessive brain activity (electrical storm) that could cause an epilepsy attack

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36
Q

How do the axons of squids differ from those of mammals? Explain the effect that this has on their function.

A

They have a big diameter, which allows for more channels to be present and have faster depolarizations

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37
Q

How do mammals make up for the small diameter of the axons of the neurons?

A

They have myelinated axons which propagates the electrical signal faster

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38
Q

Describe the structure and makeup of the myelin that surrounds vertebrate axons.

A

Myelin acts as an electrical insulator and is interrupted by periodic nodes of Ranvier

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39
Q

What is the function of the myelin and nodes of Ranvier?

A

Myelin makes the electrical signal propagate faster because less regeneration is needed whereas the Ranvier Nodes allow for the regeneration to happen periodically before the signal fades out.

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40
Q

Where are Na+ channels found along the axon?

A

In the Ranvier Nodes

41
Q

What is the cause of multiple sclerosis?

A

An autoimmune disease that detects the oligodendrocyte’s surface proteins and destroys myelin in the process. This destruction can cause loos in function.

42
Q

What is the difference between white and gray matter in the brain?

A

Gray matter in the dendrites and cell bodies while the white matter in myelinated axons

43
Q

What are the 3 broad categories of synapses?

A

Axodendritic
Axosomatic
Axoaxonic

44
Q

What is an axosomatic synapse? Is it excitatory or inhibitory or both?

A

A synapse that acts on the neuron’s cell body. It’s inhibitory

45
Q

What is an axoaxonic synapse?

A

A synapse that acts on the axon of the post synaptic cell

46
Q

What are the two types of axodendritic neurons? Explain the difference (location) between them.

A

Spine: usually excitatory
Shaft: usually inhibitory

47
Q

How does an action potential behave when it reaches a branch point? What consequence does this have on neurotransmission?

A

The same action potential will propagate on every branch, meaning that the same signal will be sent to it’s associated post synaptic cell

48
Q

Describe the major components of the structure of the synapse.

A
  1. The presynaptic terminal is the enlargement at the end of the axon.
  2. Synaptic clef is where the neurotransmitters are diffused
  3. Presynaptic vessels contain the neurotransmitters
  4. Active zone is where some vesicles are lined up
49
Q

Describe how presynaptic vesicles are organized in the presynaptic terminal.

A

Some are lined up and tethered to the membrane and will be the principal actors in the transmitting of the signal
Other vesicles are floating in the presynaptic terminal as backups if more neurotransmitters are needed

50
Q

Describe the organization of postsynaptic densities and their purpose.

A

They are concentrations of specialized proteins located in the postsynaptic spine, facing the synaptic cleft.

51
Q

What type of channels are found in the presynaptic terminal? What is their purpose?

A

There are Ca2+ voltage-gated channels. when they open, they will trigger the release of neurotransmitters

52
Q

What type of channels are found in the postsynaptic spine? What is their purpose?

A

Ligand-gated ion channels (aka neurotransmitter receptors). These are activated when the neurotransmitter binds to them.

53
Q

Describe the 3 major steps of chemical synaptic transmission.

A
  1. the action potential invades the presynaptic terminal. This opens the voltage-gated calcium channels, allowing Ca2+ to flow in.
  2. Synaptic vesicles fuse with the presynaptic membrane, releasing the neurotransmitter into the synaptic cleft.
  3. The transmitter diffuses across the cleft and activates receptors in the post-synaptic membrane. The chemical signal gets converted into an electrical signal, causing a change in the electrical properties of the postsynaptic spine.
54
Q

What is the fate of presynaptic vesicles once they have emptied their contents into the synaptic cleft?

A

they are reused for other synapses

55
Q

Explain the process by which presynaptic vesicles fuse with the membrane.

A

When the calcium channel opens, the Ca2+ flows in and binds to proteins that are part of this complex. This causes the proteins to charge their conformation, which drives the fusion of the vesicle with the presynaptic membrane.

56
Q

What are the two types of postsynaptic responses to a neurotransmitter?

A

EPSP: excitatory postsynaptic potential
IPSP: inhibitory postsynaptic potential

57
Q

What is the difference between an EPSP and an IPSP?

A

EPSP depolarizes the cell, making it more likely to produce an action potential
IPSP hyperpolarizes the cell, making it less likely to produce an action potential

58
Q

What is the main excitatory neutransmitter?

A

Glutamate

59
Q

Where is glutamate found (before an action potential is fired)?

A

It’s in vesicles inside the excitatory pre-synaptic neuron. Those are mainly brain neurons

60
Q

What are the two types of glutamate receptors found in the postsynaptic spine?

A

AMPA and NMDA receptors

61
Q

AMPA receptors and NMDA receptors are […] receptors. What does this mean?

A

ionotropic
They let in ions when they are activated (ions channels) by a molecule binding to the receptor site

62
Q

Explain how AMPA receptors work.

A

They are responsible for fast EPSP. In the absence of glutamate, they are closed. When glutamate binds on the binding site, the receptors open and let in Na+ ions, depolarizing the post-synaptic neuron

63
Q

How big is an EPSP?

A

It is very small

64
Q

How long does a typical EPSP last?

A

about 20 msec

65
Q

How many EPSPs are required to initiate an action potential? Do they all come from the same place?

A

Since they are small and quick, a neuron requires many close-in-frequency EPSPs to initiate a potential action. All these different EPSPs come from different EPSP synapses.
This is possible from multiple synapses’ action in synchrony or from an individual synapse activated at high frequency.

66
Q

Describe the key properties of NMDA receptors.

A
  1. At the resting membrane potential, the pore is blocked by an MG2+ (it is only expelled when the membrane is depolarized enough)
  2. The open pore is extremely permeable to Ca2+
67
Q

Compare the activity of ionotropic receptors during resting potential vs when depolarization occurs.
(when glutamate has bound.)

A

RESTING
NMDA: open but clogged by a Mg2+ molecule, no EPSP
AMPA: open and letting Na+ go through, EPSP

DEPOLARIZATION
NMDA: open, and Mg2+ is pushed out by the charges. Ca2+ flows in, EPSP
AMPA: open and letting Na+ go through, EPSP

68
Q

What is the purpose of the Ca2+ that flows into the postsynaptic terminal via NMDA receptors? What is this process called?

A

Ca2+ acts as a second messenger and starts cascades of signals that can contribute to long-term potentiation (LTP). This process is an example of synapses plasticity

69
Q

Which type of ionotropic receptor causes the “fast” depolarization of the postsynaptic terminal?

A

AMPA

70
Q

Explain what happens during LTP during the control phase.

A

A single excitatory signal is sent. Some glutamate is released, and the post-synaptic neuron is slightly depolarized.

71
Q

Explain what happens during LTP in the induction phase.

A

High-frequency action potentials are sent to the excitatory neuron. This highly depolarizes the postsynaptic neuron, removing the Mg2+ of NMDA receptors and enabling them to conduct Ca2+. There is an EPSP build-up that depolarises a lot. The Ca2+ brings on property changes to the neuron.

72
Q

What is the effect of induction on EPSPs in LTP?

A

Hours after the induction of LTP, the Ca2+ has caused more AMPA to go to the surface of the postsynaptic neuron. The next time a single action potential is fired (base line level) the small amount of glutamate binding to more receptors than initially will bring on a big depolarization.
(stronger than initailly)
this is the process of learning and making stronger connections

73
Q

What happens when concentrations of glutamate are too high in a neuron? when will it happen

A

Excitotoxicity. This is toxic for a neuron and is likely to happen after a stroke.
When a neuron dies from a lack of blood flow, it releases all its glutamate, which then diffuses. If the adjacent neurons have overactivated AMPA and NMDA receptors, they recognize it and die.

74
Q

What is the purpose of inhibitory synapses?

A
  1. Control the positive feedback loop created by excitatory neurons
  2. Influence the frequency of EPSP
75
Q

What is the main inhibitory neurotransmitter? Where is it found (prior to action potential)

A

GABA Is in vesicles inside the inhibitory pre-synaptic neuron. Those are mainly brain neurons

76
Q

What post-synaptic receptors are responsible for GABA?

A

GABA a receptors

77
Q

The GABA(A) receptor is an […] receptor

A

ionotropic

78
Q

Explain the function of the GABA(A) receptor.

A

They cause an influx in Cl- which hyperpolarizes the postsynaptic membrane.

79
Q

What is the most common target for therapeutic compiunds like valium and xanax?

A

GABA(A) receptors are important targets for these compounds. These drugs bind to the receptor and make it more sensitive to GABA, making inhibitory synapses work better. This is why they might make the user sleepy.

80
Q

Where are excitatory and inhibitory inputs located on a given neuron?

A

E: on the spine
I: on the shaft

81
Q

Whether or not a neuron fires an action potential depends on […]

A

the relative balance of EPSPs and IPSPs

82
Q

What determines whether a neuron is excitatory or inhibitory?

A

In the developmental stage, it is determined and stays the same

83
Q

How does the morphology of inhibitory neurons differ from excitatory neurons? Why?

A

Excitatory neurons have more dendritic branches to spread all the necessary information whereas inhibitory have shorter and less branched dendrites as they have a more localized function.

84
Q

What are the two types of receptors found in synapses?

A

Ionotropic and metabotropic

85
Q

Metabotropic receptors are called […]

A

GPCRs

86
Q

Are metabotropic receptors found in excitatory synapses, inhibitory synapses, or both?

A

in both, they are different receptors

87
Q

Describe how mGluR’s work (in an excitatory synapse).

A

When the glutamate binds to the receptor, it synthesizes and releases 2nd messenger inside the postsynaptic cell that starts a cascade of biochemical signals

88
Q

What is the purpose of second messengers?

A

They activate different proteins in the postsynaptic neuron making a slower and long-lasting response to the action potential.

89
Q

What are the metabotropic GABA receptors called?

A

GABA b receptors

90
Q

What are neuromodulators?

A

Neuromodulators aren’t directly causing action potentials. Instead, they act on excitatory or inhibitory neurons to modify their behavior—for example, by increasing or decreasing their responsiveness to other neurotransmitters. This modulation can make neurons more or less likely to fire in response to future signals, thereby regulating the overall excitability or strength of neural circuits without directly triggering immediate synaptic transmission.

91
Q

Give 3 examples of neuromodulators.

A

dopamine, serotonin, Norepinephrine (Noradrenaline)

92
Q

What types of neurons release neuromodulators?

A

small brainstem or midbrain nuclei that branch far into the brain to affect the cerebral cortex

93
Q

What is the role of norepinephrine?

A

It enhances alertness or attention and plays a role in the wake cycle.

94
Q

What is the role of serotonin?

A

influences our mood

95
Q

What is the role of dopamine?

A

modulates learning and it’s close relation to rewards

96
Q

How does the duration of the effects of metabotropic receptors compare to the duration of an action potential? Explain.

A

They are longer since the cascade of signal can reach many proteins, unlike glutamate or GABA, which is quickly removed.

97
Q

Explain how drugs might interact with neuromodulator systems.

A

They can bind to the same place as the neuromodulator and so create a similar response but artificially.

98
Q

How does prozac interact with neuromodulator systems?

A

they affect the serotonergic tranmission

99
Q

How do amphetamines, cocaine, and other stimulants interat with neuromodulator systems?

A

they affect the norepinephrine transmission