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Cell Biology > Synapse > Flashcards

Synapse Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What are the 2 fundamentally different functions of the neurons?

A

In dendrites towards the cell body and in axons away from the cell body.

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2
Q

What is the stem of the axon from the cell body called?

A

The axon hillock.

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3
Q

What is the potential on the inside of a neuron?

A

Negative 70. The resting membrane potential.

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4
Q

What instrument measures the potential of a neuron?

A

Measured using a glass electrode.

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5
Q

What are the properties of an action potential?

A

Self propagates and travels in one direction.

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6
Q

How are action potentials graded?

A

By frequency.

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7
Q

What is the apex of the neuron?

A

The axon.

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8
Q

Where does secretion of chemicals occur in a neuron?

A

At the axon terminal.

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9
Q

What is the base of a neuron?

A

The dendrites.

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10
Q

What are synapses?

A

Specilised regions of close approach between axon and another cell.

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11
Q

What is the axon end bulb?

A

The site of chemical neurotransmitter release.

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12
Q

What are the microtubules in the pre-synaptic membrane for?

A

Vesicle transport.

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13
Q

What is the synaptic cleft?

A

The gap which is after the presynaptic cell and before the postsynaptic cell.

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14
Q

What is a bouton?

A

The terminal of the presynaptic cell forms a swelling called a bouton.

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15
Q

How big is the synaptic gap?

A

20nm

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16
Q

How do dendrites increase surface area?

A

Through dendrite trees and dendritic spines.

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17
Q

How does the vesicles and presynaptic membrane recognise each other?

A

V-snare on vesicle complexes with t-snare at presynaptic membrane

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18
Q

What happens when the v-snare and t-snare binds?

A

The complex folds strongly and draws the membranes close.

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19
Q

What causes exocytosis of the vesicle?

A

Calcium induces synaptotagmin to displace complexin and exocytosis proceeds.

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20
Q

Where are peptide neurotransmitters made?

A

In the RER and packaged into vesicles in the Golgi.

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21
Q

Where are small molecular neurotransmitters found?

A

Made locally then imported into the vesicle.

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22
Q

What are the 2 types of receptors for NTs on the postsynaptic membrane?

A

Ionotropic receptors and metabotropic.

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23
Q

What do ionotropic receptors allow?

A

Fast signals.

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24
Q

What are metabotropic receptors?

A

Slow signals.

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25
Q

What happens when a NT binds to an ionotropic receptor?

A

A conformational change is induced.

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26
Q

Which NTs can bind to ionotropic receptors?

A

Ach, GABA and glutamate.

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27
Q

What was the opening of pores visualised by?

A

Cryo-electron microscopy.

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28
Q

What is the function of the G protein complex?

A

To bind GTP and hydrolyse it to GDP.

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29
Q

How fast is a metabotropic receptor?

A

100ms to minutes.

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30
Q

What is the initial step in the metabotropic receptor?

A

The receptor bind the G-protein and GTP replaces GDP.

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31
Q

What is the second step in the metabotropic receptor?

A

Active G-protein leaves and binds to the target enzyme.

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32
Q

What is the third step in the metabotropic receptor?

A

Enzyme generates the messenger and the messenger binds to the channel to open it.

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33
Q

What is the fourth step in the metabotropic receptor?

A

GDP-ase removes Pi from GTP and inactivates the G protein.

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34
Q

What is the penultimate step in the metabotropic receptor?

A

G protein leaves the enzyme and inactivates it.

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35
Q

What is the final step in the metabotropic receptor?

A

G protein is free and ready to bind to the receptor again.

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36
Q

What can detect the release of single vesicles?

A

Electrophysiology.

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37
Q

What have electrophysiological experiments shown?

A

That the release of neurotransmitters is quantal (in packets).

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38
Q

What does quanta relate to?

A

The release of contents of single vesicles at the presynaptic membrane.

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39
Q

What does the strength of signal correlate to?

A

The more vesicles released, the stronger the signal at the postsynaptic membrane.

40
Q

What are postsynaptic potentials caused by?

A

The passage of ions through ion channels which have opened following receptor interactions.

41
Q

Why would a response be called excitatory?

A

A net flow of positive ions into the cell depolarises the membrane and is thus called excitatory.

42
Q

What is the amplitude of the signal related to?

A

For both inhibitory and excitatory PSPs the amplitude of the signal decreases with distance as well as time.

43
Q

What are the different types of summation?

A

Spatial and temporal.

44
Q

What is spatial summation?

A

Multiple neurons stimulating the same postsynaptic membrane.

45
Q

What is temporal summation?

A

Same neuron with multiple action potentials.

46
Q

What does EPSP stand for?

A

Excitatory postsynaptic potential.

47
Q

What does IPSP stand for?

A

Inhibitory postsynaptic potential.

48
Q

Do EPSPs propagate?

A

They do not actively propagate along the axon.

49
Q

What can cause EPSPs?

A

By direct (ionotropic) or indirect (metabotropic) gating.

50
Q

Why can EPSPs summate?

A

EPSPs have no refractory period thus a series of EPSPs can summate.

51
Q

What can cause an action potential?

A

What can cause an action potential?

52
Q

What does the strength of the PSP depend on?

A

Placement and excitatory or inhibitory nature of the inputs.

53
Q

What determines the level of excitation?

A

Dendrite structure and synapse location.

54
Q

What does dendritic spine morphology influence?

A

PSP summation.

55
Q

What does PSP stand for?

A

Post synaptic potential.

56
Q

Does dendritic spine length influence EPSP summation?

A

The longer the spine the lower the EPSP.

57
Q

What are EPSPs and IPSPs important in?

A

They are passive electrical activity important for setting the axonal response.

58
Q

What are the other forms of electrical activity in the dendrites?

A

Self propagating dendritic spikes.

59
Q

What does the dendritic spike do?

A

Boost the depolarization in the dendrites.

60
Q

When do dendritic cells occur?

A

Especially when stimulation is intense in space or time.

61
Q

How can dendritic spikes stimulate an action potential?

A

They can leak into the cell body to stimulate an AP.

62
Q

Do dendritic spikes act locally?

A

They are thought to act locally on postsynaptic membranes to generate LTP.

63
Q

What is memory due to?

A

Strengthened synapses and making of new synapses.

64
Q

What is required to reach the threshold?

A

Spatial and temporal summation of multiple PSPs/dendritic spikes.

65
Q

What does stronger synapses result in?

A

Increased: NT release, sensitivity, number of receptors and size of post synaptic machinery.

66
Q

What does LTP stand for?

A

Long term potentiation.

67
Q

What is LTP associated with?

A

Making new synapses in vivo.

68
Q

How are stronger synapses formed?

A

Upregulation of NT secretion and receptor expression.

69
Q

How are more synapses made?

A

Sprouting, branching and dendritic spine formation.

70
Q

What is Hebb’s learning rule about correlation?

A

Correlated pre and postsynaptic activities cause synapse to strengthen.

71
Q

What is Hebb’s learning rule about uncorrelation?

A

Uncorrelated pre and postsynaptic activities cause synapse weakening.

72
Q

Why could synaptic change occur?

A

Because of neuronal activity at critical points within a behavioral brain pathway.

73
Q

What is a good example of changes in behavioral learning?

A

Addiction.

74
Q

What could be these synaptic changes?

A

Increases and decreases in synaptic strength leading to behavioral plasticity.

75
Q

How can drugs be addictive?

A

Drugs can cause massive release of dopamine in the reward centre.

76
Q

What starts the behavioral changes when introduced to an addictive drug?

A

Synaptic plasticity in glutaminergic synapses.

77
Q

What is the reward centre?

A

The nucleus accumbens.

78
Q

What are the types of inhibition in multi-neuron networks?

A

Lateral inhibition, feedforward inhibition, feedback inhibition.

79
Q

What are the types of excitation in multi-neuron networks?

A

Feedforward and feedback/recurrent.

80
Q

What start the knee jerk reflex?

A

By tapping the tendon connected to the quadricep which stretches the muscle.

81
Q

Describe pyramidal cell firing.

A

It is under strict time control to prevent run away excitation.

82
Q

How are the pyramidal cells inhibited?

A

Done by feedforward and feedback inhibition.

83
Q

What do inhibitory microcircuits involve?

A

Interneurons and short axons.

84
Q

What are the properties of inhibitory microcircuits?

A

Fast acting and inhibition is mostly by GABA.

85
Q

Where are central pattern generators?

A

In the spinal cord.

86
Q

What are the central pattern generators used in?

A

Communication in white matter in spinal cord.

87
Q

What is an example of central pattern generators?

A

Alternating rhythms for walking generated in the spinal cord.

88
Q

What is an example of inhibitory interneurons for pain?

A

Stimulation of touch can help to block transmission of pain impulses to the brain.

89
Q

How can touch decrease pain?

A

Touch fibres stimulate inhibitory interneurons to decrease activity in axons of pain fibres.

90
Q

What affects the degree of convergence?

A

The more dendrites a neuron has, the higher the degree of convergence.

91
Q

What are examples of neuronal convergence in a circuit?

A

Pyramidal cells and Purkinje fibres.

92
Q

What are pyramidal cells?

A

A type of multipolar neuron found in areas of the brain.

93
Q

Where in the brain are pyramidal cells found?

A

The cerebral cortex, hippocampus and amygdala.

94
Q

What is neuronal divergence?

A

Information from a single neuron is passed to a number of other neurons simultaneously.

95
Q

How is sensory information diverged?

A

Sensory information arriving at the somatosensory cortex can be diverged widely through the cortex.

Cell Biology (20 decks)

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