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SMP - MCP Exam 2 > Lecture 23: Synaptic Physiology > Flashcards

Lecture 23: Synaptic Physiology Flashcards

1
Q

What is an electrical synapse?

A

Physical connections or gap junctions between the pre and postsynaptic membranes
Does not involve NTs

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2
Q

Which are faster: electrical or chemical synapses? Why?

A

Electrical because they are only delayed by the time it takes for the ion current to flow through the gap junction whereas chemical synapses need to way for calcium to enter, NTs release, NTs travel and bind, and ion currents created.

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3
Q

How much slower is the chemical synaptic delay compared to the electrical synaptic delay?

A

10 times slower

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4
Q

What are electrical synapses used for in the CNS? What creates these APs?

A

To increase the global activity of the early developing nervous system = tons of uncoordinated movements (these synapses disappear when motor coordination is established)
Calcium waves create these movements

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5
Q

What are central synapses?

A

Chemical synapses in the CNS

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6
Q

What kind of synapses happens at the NMJ?

A

Chemical synapses

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7
Q

How does the number of paired connexons in a gap junction affect synaptic coupling?

A

LESS resistance = stronger synaptic coupling

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8
Q

How can one measure the efficacy of electrical synapse? What is needed for this?

A

CURRENT CLAMP EXPERIMENT:
By injecting current into a pre-synaptic cell and measuring the voltage in both the pre (depends on membrane resistance and Ohm’s law) and post-synaptic cells (depends on resistance of connexons)
Calcium inhibitors to prevent muscle contractions

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9
Q

Why is voltage in the postsynaptic cell lower than in the presynaptic cell?

A

Because of resistance of gap junctions = how many connexons are active

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10
Q

What is the NMJ?

A

The synapse between a motor neuron (that extends from the CNS to the PNS) and a muscle cell

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11
Q

What is the neurotransmitter responsible for EPSPs in central synapses?

A

Glutamate

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12
Q

Where are glutamate receptors located on the CNS postsynaptic cell?

A

Dendritic spines or shafts, or in the soma (neuron body)

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13
Q

Where are inhibitory chemical synapses NEVER found?

A

Dendritic spine

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14
Q

What does GABA stand for?

A

gamma-aminobutyric acid

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15
Q

Do central synapses have a safety factor? What does this mean?

A

NOPE, they are no very efficacious

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16
Q

What are the neurotransmitters responsible for IPSPs in central synapses?

A

GABA (in brain) and glycine (in spinal cord)

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17
Q

Are there specific enzymes that can degrade NTs in central synaptic clefts?

A

NOPE

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18
Q

What are the 7 main differences between central synapses and those at the NMJ?

A
  1. Types of possibile synapses
  2. NTs
  3. Number/position of presynaptic release sites
  4. Number of postsynaptic receptors
  5. Efficacy of presynaptic release
  6. Enzymes to degrade NTs
  7. Physical structure
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19
Q

Can a presynaptic neuron produce both GABA and glutamate?

A

No

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20
Q

Can a postsynaptic neuron have both GABA and glutamate receptors?

A

Yes

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21
Q

Where are the release sites on the central presynaptic cell?

A

Multiple sites all along the axon

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22
Q

How many chemical postsynaptic receptors at each site compared to the NMJ?

A

Few: about 100/site

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23
Q

What are the main ways to remove NTs in central synapses?

A

Diffusion and reuptake

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24
Q

How does the brain regulate the intensity of synaptic transmission? What is this called?

A

By activating multiple excitatory and inhibitory synapses at the same time: summation

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25
Q

What is the axon hillock? What is special about this spot?

A

Specialized part of the cell body (or soma) of a neuron that connects to the axon: where summation of APs converge

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26
Q

What theory has been proposed to explain what mental illnesses derive from?

A

Some GABAergic synapses are found on the axon hillock and are easier to inhibit

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27
Q

What is temporal summation?

A

The summation of two synapse potentials close together in time

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28
Q

What is space summation?

A

The summation of two synapse potentials close together in space

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29
Q

What is the temporal summation regulated by?

A

The time constant = Rm.Cm: the larger the time constant, the more temporal stimulation happens because they have more time to add up

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30
Q

What is the spatial summation regulated by?

A

The space constant = SR(Rm/Ri): the larger the space constant, the more spatial summation happens because far apart potentials can be added up

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31
Q

What does the effect of spontaneous synaptic transmissions depend on?

A

The number of receptors on the post-synaptic cell

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32
Q

How can one study the chemical synaptic transmission?

A

Patch-clamp experiments to study the behavior of specific ion channels based on different NT concentrations

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33
Q

What are MINIs?

A

Miniature Spontaneous Synaptic Events (chemical) = spontaneous release of 1 vesicle (quanta)

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34
Q

How can one study MINIs?

A

Use TTX, TEA, or curare and record synaptic events

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35
Q

How does the quantal size relate to MINIs?

A

Quantal size = average MINIs amplitude

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36
Q

How can one calculate the quantal content?

A

M = mean amplitude of responses / quantal size

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37
Q

What do quantal size and content characterize?

A

The strength of the synapse and the relative contribution of pre and postsynaptic efficacy

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38
Q

How many receptors activated by 1 vesicle in a central synapse?

A

4-5

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39
Q

What are the 3 types of glutamate receptors?

A

AMPA, NMDA, and Kainate

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40
Q

What kind of receptors are glutamate receptors?

A

Ionotropic ligand gated ion channels for positive ions (domain 2)

41
Q

What kind of receptors are GABA/glycine receptors?

A

Ionotropic ligand gated ion channels for negative ions (domain 2)

42
Q

How many subunits in glutamate receptors?

A

4

43
Q

How many subunits in GABA/glycine receptors?

A

5

44
Q

What are the 2 main types of brain NTs?

A

Fast/Localized: GABA/glycine and glutamate

Slow/sprinker: mood, anxiety, feelings etc

45
Q

What is GABA’s antagonist?

A

Bicuculline

46
Q

What is glycine’s antagonist? What does it cause?

A

Strychnine (rat poison): seizure

47
Q

What kind of receptors do slow NTs activate?

A

Metabotropic (GTP binding proteins)

48
Q

What is the speed of the current through AMPA receptors?

A

Very fast

49
Q

What are AMPA receptors permeable to once activated? What does this mean for their Erev?

A 
Na+/K+
0 mV (same as AChRs)
50
Q

What are NMDA receptors permeable to once activated?

A

Calcium, K+/Na+

51
Q

Describe NMDA receptor activation to Erev (5 steps)

A
  1. Glutamate and glycine (co-activator)
  2. Na+ rushes in
  3. Magnesium removed from NMDA channel (this is voltage dependent)
  4. Calcium rushes in
  5. K+ rushes out
52
Q

What is the effect of calcium permeability on NMDA channels?

A

Cause strong depolarization that plays a role in memory formation (long term potentiation)

53
Q

What are the kinetics of NMDA receptors like?

A

Slow: take long to activate and deactivate (open for longer than AMPA channels)

54
Q

What does excessive amounts of glutamate in the brain cause? Why? In what circumstances does this happen?

A

Toxic to neurons and may even cause cell death because of the excessive calcium influx in NMDA receptors causing activation of calcium sensitive proteases and lipases and generation of free radicals

Stroke (ischemia), hypoglycemia, traumatic injury, repeated seizures

55
Q

What are many forms of epilepsy due to? What is the treatment?

A

Alterations of GABA receptors (Cl- transport mechanism) cause chloride concentrations to drop in the cell and GABA becomes excitatory so too much excitation!
Drugs to enhance the GABA receptors.

56
Q

What central synapse receptors are often the underlying cause of sleep and anxiety disorders?

A

Alterations in GABAa receptors

57
Q

What kind of meds increase the function of GABA channels? Through what kind of action?

A

Axiolytics, tranquilizers, general anesthetics

Allosteric stimulation

58
Q

When you have a graph of membrane potential vs EPSP, what is the slope equal to?

A

Resistance of the membrane

59
Q

What is the Erev of EPSPs?

A

0 mV

60
Q

What does the Erev of IPSPs depend on?

A

[Cl]in and [Cl]out

61
Q

What is the effect of magnesium on the EPSP of NMDA receptors?

A

Negative slope between -80mV and -40 mV

62
Q

Is the AMPA channel voltage dependent?

A

Nope

63
Q

How long can slow EPSPs and IPSPs last?

A

Several seconds or even minutes

64
Q

What is the purpose of having inhibitory potentials?

A

Because of spontaneous potentials

65
Q

Explain the knee-jerk reflex.

A

Stretch reflex in our patella tendon:
1. Hit the patella tendon with a reflex hammer inducing a stretch in the muscle spindle of the quadriceps muscle.
2. Sensory neuron fires and carries the signal to the spinal cord where it synapses with an excitatory motor neuron and an inhibitory interneuron
3. The excitatory motor neuron generates an
EPSP which synapses with the extensor muscle.
4. The inhibitory
interneuron generates an IPSP that continues down the flexor motor
neuron to synapse with the flexor muscle.
5. Contraction occurs in the extensor muscle and
relaxation occurs in the flexor muscle.

66
Q

Explain the knee-jerk reflex.

A

Stretch reflex in our patella tendon:
1. Hit the patella tendon with a reflex hammer inducing a stretch in the muscle spindle of the quadriceps muscle.
2. Sensory neuron fires and carries the signal to the spinal cord where it synapses with an excitatory motor neuron and an inhibitory interneuron
3. The excitatory motor neuron generates an
EPSP which synapses with the extensor muscle.
4. The inhibitory
interneuron generates an IPSP that continues down the flexor motor
neuron to synapse with the flexor muscle to make sure the reflex is unopposed.
5. Contraction occurs in the extensor muscle and
relaxation occurs in the flexor muscle.

67
Q

What is a muscle spindle?

A

Sensory receptors within the belly of a muscle that primarily detect changes in the length of this muscle

68
Q

Is the brain involved in the knee-jerk reflex?

A

No - it receives info about it after

69
Q

What % of synapses in the entire NS are glutamatergenic?

A

70%

70
Q

What is an interneuron?

A

Neuron where both soma and axon are contained in the spinal chord

71
Q

How do the synapses in the NS differ from those at the NMJ?

A

One synapse potential in the NS can be produced by many axons

72
Q

How is the lack of safety factor overcome in the CNS?

A

The number of presynaptic cells!

73
Q

What happens postsynaptically when an inhibitory action potential is fired?

A

Hyperpolarization due to Cl- coming in or K+ going out

74
Q

What is the memory of the phone? Chip: transistor: electronical device with two states: 0 or 1. Every picture is either 0 or 1

A

Equivalent of transistor is the efficacy of the excitatory synapse.

75
Q

How many genes code for connexins?

A

Many

MANY DISEASES DUE TO MUTATIONS ON THESE

76
Q

How many genes code for connexins?

A

Many

MANY DISEASES DUE TO MUTATIONS ON THESE

77
Q

Describe the movement of a gap junction?

A

All 12 connexins move in synchrony allowing an electrical signal to go through

78
Q

Can both a hyperpolarization and a depolarization be communicated via gap junctions in an electrical synapse?

A

YUP

79
Q

What are the physical differences between an NMJ and a central synapse?

A

Central synapses occur en passant along the same axon vs NMJ synapses occur at terminal bouton (presynaptic terminal)

80
Q

What are dendritic spines?

A

Small membranous protrusion from a neuron’s dendrite that typically receives input from a single axon at the synapse.

81
Q

What is the neuron’s dendrite?

A

Part of the neuron receiving APs

82
Q

What organ generates the most electricity?

A

The heart (left ventricle)

83
Q

Why can spontaneous synaptic transmissions on the same synapse create different ion currents?

A

Because they are produced at different points on the cell where the number of channels is different

84
Q

How can blocking presynaptic K+ voltage-gated channels increase quantal content?

A

Because repolarization would not happen and AP will be longer, causing the calcium channels to be open for longer

85
Q

Are there nicotinic receptors in the brain? If so, what is their function?

A

Yes: not well understood and have different subunits than those at the NMJ

86
Q

In what kind of experiments in the Erev studied?

A

Voltage clamp experiments

87
Q

What happens if you increase the intracellular concentration of all neurons?

A

You transform every inhibition in the brain into excitation

88
Q

Chloride coming in the cell to depolarize it: outward or inward current?

A

Outward current!

89
Q

Inward current carried by NEGATIVE ion is inward or outward current?

A

Outward!

90
Q

Outward current carried by NEGATIVE ion is inward or outward current?

A

Inward!

91
Q

Outward current carried by POSITIVE ion is inward or outward current?

A

Outward

92
Q

Inward current carried by POSITIVE ion is inward or outward current?

A

Inward

93
Q

How are very slow EPSPs and IPSPs produced?

A

By enhancing or inhibiting leakage channels

94
Q

What are the 3 receptors for slow EPSPs and IPSPs?

A

Muscarinic, dopaminergic , norepinergic

95
Q

What can affect quantal size? 4 factors

A
  1. Number of receptors on postsynaptic cell
  2. Average open time of the receptors on the postsynaptic cell
  3. Conductance of the receptors on the postsynaptic cell
  4. Concentration of neurotransmitters in a vesicle
96
Q

What are 2 ways of inhibiting a postsynaptic cell?

A
  1. Gap junction

2. GABA receptors

97
Q

What are calcium waves?

A

Calcium oscillations in unitary smooth muscles: calcium enters the cell and then K+ channels activated by calcium repolarize the muscle

98
Q

What is a common feature of all smooth muscle action potentials?

A

They are all very slow compared to skeletal muscle APs!

99
Q

What does increased intracellular concentration of chloride do to GABArgenic neurons?

A

Membrane depolarization

SMP - MCP Exam 2 (13 decks)

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