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Flashcards in Synaptic transmission Deck (133)
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1
Q

What are the two types of synapses?

A

Electrical

Chemical

2
Q

What are the two types of chemical synapses?

A

Neuron-neuron

Neuron-muscle

3
Q

Electrical synapses are made up of what membrane proteins? Where are these from (which cells)?

A

Connexons–one from each neuron participating in the synapse

4
Q

How many connexins make a connexon?

A

6

5
Q

Are most electrical synapses uni or bidirectional?

A

Bidirectional

6
Q

How fast are electrical synapses?

A

Extremely fast

7
Q

Why do electrical synapses have a low selectivity?

A

Connexons allow water and ions to pass through without any specific selection (size is only selection)

8
Q

How do electrical synapses relate to chemical synapses?

A

They mediate chemical synapses

9
Q

What are the four ways that neurons can transmit chemical signals?

A
  1. Endocrine
  2. Paracrine
  3. Synaptic
  4. Autocrine
10
Q

What is autocrine signalling for neurons?

A

Receptors on pre-synaptic cell for transmitter it releases

11
Q

What is a neuromodulator?

A

chemical messenger that can affect release of neurotransmitter or the receptor function of a neurotransmitter. Some chemicals can be both neurotransmitters and neuromodulators.

12
Q

What is paracrine signalling?

A

Signals released to local cells

13
Q

What organelle is always found in presynaptic synapses?

A

Mitochondria b/c there is a high energy need

14
Q

Are neurotransmitters in presynaptic neurons made on the spot or are they stored?

A

Stored in vesicles

15
Q

The influx of what ion leads to release of the neurotransmitters in vesicles?

A

Ca

16
Q

What are the transmembrane proteins that hold chemcial synapses togehter?

A

Neurexins

17
Q

Are chemical synapses unidirectional, or bidirectional?

A

Unidirectional

18
Q

True or false: in influx of Ca ions in the presynaptic bouton causes a moderate-major change in [Ca]

A

False-very small and localized

19
Q

The increase in [Ca] in the presynaptic bouton causes what to happen?

A

Release of neurotransmitters

20
Q

True or false: the neurotransmitter that is released from the presynaptic bouton always causes channels in the postsynaptic cleft to open

A

False–can open or close

21
Q

What are the steps in the recovery phase of a chemical synapse? (3)

A
  1. Repolarization of presyapse via K= efflux
  2. Ca channels close
  3. Ca removed from cleft
22
Q

What are the roles of SNARE proteins in synaptic transmission? (2)

A

Form a complex between the vesicle and the presynaptic cell membrane

Sensors of Ca

23
Q

How is Ca removed from its localized position in the presynaptic neuron? (4)

A
  1. Diffusion
  2. Ca binding proteins
  3. Transported into internal Ca stores
  4. Pumped out
24
Q

How are the vesicles recycled in presynaptic membranes?

A

Through clatharin mediated endocytosis

25
Q

Why is it possible to deplete chemical neurons?

A

It takes 1 minute to replenish vesicles

26
Q

What are the three major small-molecule neurotransmitters?

A

Amino acids
Acetylcholine
Amines

27
Q

What are the two different type of amines that are neurotransmitters?

A

Monoamines

Catecholamines

28
Q

What are the two responses to neurotransmitter binding on the postsynaptic bouton? What are the two processes that can take place?

A

excitation or inhibition

Depolarization or chemical cascade

29
Q

What are ionotropic receptors?

A

Ligand gated ion channels on the postsynaptic membrane

30
Q

What are metabotropic receptors?

A

G-protein coupled receptors

31
Q

Are metabotropic receptors faster or slower acting than ionotropic receptors?

A

Slower

32
Q

True or false: A postsynaptic neuron can have receptors for more than one kind of neurotransmitter

A

True

33
Q

The major excitatory neurotransmitter in the brain and spinal cord is of what type?

A

Glutamate

34
Q

What is the pore that glutamate opens? Which way do ions flow?

A

Na/K pore, which lets some K out, but a lot of Na in

35
Q

What happens to the postsynaptic neuron when glutamate binds to its channel (depolarization or hyperpolarization)?

A

Depolarization (d/t net influx of Na) and thus excitation

36
Q

What does it mean that the depolarization caused by a single glutamate receptor is decremental?

A

It is only local, and will not elicit a depolarization event by itself

37
Q

What is the primary inhibitory neurotransmitter in the nervous system?

A

GABA

38
Q

True or false: Metabotropic receptors can cause excitatory effects in several ways

A

True

39
Q

Ionotropic GABA receptors are permeable to what ion? What happens when these open?

A

Cl-

This causes CL to flow down its [C] gradient into the neuron, and hyperpolarize it

40
Q

 If ECl- is more negative than resting membrane potential, which is the case for most neurons, then increasing Cl- permeability causes Cl- to flow where?

A

Into the cell

41
Q

What would happen to a postsynaptic neuron if a metabotropic receptor caused K channels to open (and a subsequent efflux of K)?

A

Hyperpolarization

42
Q

How can metabotropic receptors effect a depolarization through K or Cl channels?

A

Decrease the permeability of the channels

43
Q

What is a synaptic delay?

A

Time interval between when action potential invades the pre-synaptic terminal and when a membrane potential change begins in the post-synaptic cell

44
Q

Which type of synapse has a longer delay: chemical or electrical?

A

Chemical

45
Q

What are the three ways in which transmitters are removed from the synaptic cleft?

A

Diffusion
Enzymatic degradation
Reuptake/transport

46
Q

What is the MOA of cocaine?

A

Binds to the dopamine reuptake protein ono the presynaptic neuron, and prevents reuptake

47
Q

What is the target of SSRIs?

A

5HT transporters

48
Q

What is the target of MAOIs?

A

Monoamine oxidase (the enzyme that oxidizes 5HT

49
Q

What is the target of TCA (tricyclic antidepressants)

A

5HT transporter

50
Q

What is temporal summation?

A

When the same presynaptic neuron gives a signal in rapid succession to elicit a response in the postsynaptic neuron

51
Q

What is spatial summation?

A

When two or more separate neurons create signals that are given together to elicit a postsynaptic response

52
Q

What is synaptic efficacy?

A

how big an effect a synapse has on the postsynaptic cell.

53
Q

What is synaptic plasticity?

A

“the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity” - wiki

54
Q

What is a neuromuscular junction?

A

A specialized synapse between a motoneuron and a muscle fiber

55
Q

Where does the mylein sheath end in a neuronmuscular juncation?

A

Just before the synaptic bouton

56
Q

What is the major difference in neuromuscluar junction presynapses, as compared to CNS synapses?

A

There are multiple active zones within the presynaptic terminal

57
Q

What organelle is found in high amounts in the presynaptic terminal of a neuromuscular junction?

A

Mito

58
Q

What is the major difference in neuromuscluar junction postynapses, as compared to CNS synapses? What is the purpose of this?

A

There are many junctional folds

59
Q

What is the only neurotransmitter found in neuromuscular junctions? Receptor?

A

Acetylcholine and its nicotinic receptor

60
Q

What is the MOA of nicotinic acetylcholine receptors?

A

Allows for the influx of Na (and smaller efflux of K), activating Na channels elsewhere

61
Q

How is acetylcholine degraded?

A

Acetylcholine esterases

62
Q

What is the end plate depolarization?

A

The depolarization that takes place in neuromuscular junctions

63
Q

What is the function of anticholinesterases?

A

Inhibit acetylcholine esterase, and prolong the EPP

64
Q

Why are neuromuscluar junctions considered “safe and reliable”?

A

since in a normal, healthy person an action potential in the motor neuron always causes an action potential in the skeletal muscle fibers it synapses on

65
Q

Why is reuptake of choline essential for motor neurons?

A

This is necessary since motor neurons cannot synthesize choline and choline does not pass through cell membranes easily.

66
Q

What type of receptor is the nicotinic acetylcholine receptor? What are the ions that this uses, and how?

A

Ligand gated channel (ionotropic).

Increases permeability of K and Na, but more so to Na

67
Q

What type of channel is used in the reuptake of acetylcholine?

A

Secondary active synporter (with Na as the opposing ion)

68
Q

How many motor neurons innervate a skeletal muscle?

A

One, and only one

69
Q

Are there inhibitory synapses at neuromuscular junctions?

A

No–ONLY excitatory

70
Q

When you talk about inhibiting a skeletal muscle cell this means what?

A

that the alpha motor neuron innervating that cell is inhibited.

71
Q

Why do neuromuscular junctions need to ensure that the signal they send is strong (which they do via multiple terminals, multiple active zones, etc.)?

A

Becauses there is a 1-1 ratio of motor neurons to muscle fibers

72
Q

What is the MOA of botulina toxins? What are the symptoms of botulina poisoning?

A

Proteinase that cleaves the SNARE complex associated with vesicles in the presynaptic neuron. Thus vesicles will not be held near the end of the synapse

Symptom = flaccid paralysis

73
Q

What is the MOA of tetanus?

A

Cleaves the SNARE protein of glycine neurotransmitters (interneurons) of neurons in the spinal cord

74
Q

What is Eaton-Lambert syndrome?

A

An autoimmune attack on voltage – gated Ca++ channels in the terminals of somatic motor nerves. This inhibits vesicle release

75
Q

What is the MOA of myasthenia gravis?

A

autoimmune disease which reduces the number of acetylcholine receptors at the postsynaptic neuromuscular junction

76
Q

What is the autoimmune disease discussed in lecture that affects presynaptic channels?

A

Eaton-Lambert syndrome

77
Q

What is the autoimmune disease discussed in class that affects postsynaptic channels?

A

Myasthenia gravis

78
Q

What is the MOA of neostigmine in treating myasthenia gravis?

A

Reversibly inhibits acetylcholine esterase

79
Q

Where does the muscle weakness of Myasthenia gravis usually appear?

A

In the face

80
Q

What are the signs/symptoms of myasthenia gravis?

A

Muscle weakness, especially if it gets worse in the day.

Neck weakness against physician’s force

81
Q

What is the MOA of nicotine?

A

Agonist of the nicotinic acetylcholine receptors

82
Q

What is the MOA of bungaroo toxin? Symptoms?

A

Irreversible binding/blocking of nicotinic acetylcholine receptors. Causes paralysis

83
Q

What is edrophonium used for? MOA?

A

Used to diagnose myasthenia gravis.

Short acting, reversible cholinesterase inhibitors

84
Q

What is the MOA of sarin?

A

Irreversibly binds acetylcholine inhibitors

85
Q

True or false: irreversible inhibition of acetylcholine receptors is always poisonous

A

True

86
Q

What are the three features a neurotransmitter must have to be defined as a neurotransmitter?

A
  1. Packed into a vesicle
  2. Ca-dependent release
  3. Binds to specific receptors
87
Q

What are the three major categories of neurotransmitters?

A
  1. Small molecule
  2. Neuroactive
  3. Gaseous neurotransmitters
88
Q

What is the unconventional neurotransmitter that does not fit into the three major classes of neurotransmitters?

A

Endocannabinoids

89
Q

Which class of neurotransmitter is Acetylcholine?

A

Small molecule

90
Q

What is the receptor for acetylcholine at neuromuscular junctions?

A

Nicotinic acetylcholine receptor

91
Q

What are the two major types of acetylcholine receptors?

A

Nicotinic (fast, ionotropic)

Muscarinic (slow, metabotropic)

92
Q

Which type of neurotransmitters are biogenic amines classified as?

A

Small molecule

93
Q

What are the three biogenic amines?

A
  1. Catecholamines
  2. Serotonin
  3. Histamine
94
Q

What are the three catecholamines discussed in lecture?

A

Dopamine
Norepi
Epi
(all share common Y derivation)

95
Q

What type of receptors for epi and norepi bind to?

A

Adrenergic/noradrenergic receptors

96
Q

What defines a catecholamine? Is 5HT a catecholamine?

A

All share a common Y derivative

5HT is NOT a catecholamine, but is a biogenic amine

97
Q

What type of neurotransmitter is serotonin? What amino acid is it derived from?

A

biogenic amine

Derived from W

98
Q

What type of neurotranmitter is histamine?

A

biogenic amine

99
Q

What are the amino acid neurotransmitters?

A
  1. GABA
  2. Glycine (G)
  3. Glutamate (E)
  4. Aspartate (D)
100
Q

What is the major inhibitory neurotransmitter?

A

GABA

101
Q

What are the two main classes of GABA?

A

A and B

102
Q

What is the receptor for GABAa?

A

ligand gated Cl- channel

103
Q

What is the receptor for GABAb?

A

a metabotropic receptor which has an inhibitory effect by opening K+ channels or suppression of Ca++ channels.

104
Q

What is the efffect of glycine (inhibition or excitation)?

A

Inhibition

105
Q

What type of receptor does Glycine bind to?

A

Ion gated Cl- channel

106
Q

What is the effect of strychnine?

A

Blocks Glycine receptors

107
Q

What are the two excitatory amino acid transmitters?

A

E and D

108
Q

What are the three different classes of glutamate receptors?

A

AMPA
Kainate
NMDA

109
Q

What ion blocks the NMDA in Glutamate pathways until the postsynaptic membrane is slightly depolarized through stimulation of other excitatory receptors.

A

Mg

110
Q

The NMDA receptor channel (that binds glutamate) is permeable to what three ions?

A

Ca, Na, and K

111
Q

What receptor is believed to have an important role in memory and learning

A

Glutamate

112
Q

What is excitotoxicity?

A

Destruction of neurons by an unusually high accumulation of glutamate and related compounds

113
Q

What are the four types of “small molecule” neurotransmitters?

A

Acetylcholine
Amino acids
Purines
Biogenic amines

114
Q

What are the purine neurotranismitters?

A

ATP and Adenosine

115
Q

Is adenosine stored in vesicles?

A

No

116
Q

What is the general effect of adenosine?

A

Depressant

117
Q

What is the MOA of caffeine, theophylline, and theobromine?

A

All block adenosine

118
Q

What are the receptors for adenosine called?

A

Adenosine receptors

119
Q

What does ATP (as a neurotransmitter) bind to

A

P-type purinergic receptors

120
Q

Where are peptide precursor molecules that act as neurotransmitters synthesized? Where do they complete their maturation?

A

Synthesized in the nucleus, then packed into vesicles with enzymes and sent down neuron where they mature

121
Q

Where are small molecule neurotransmitters usually synthesized?

A

At the end of the axon

122
Q

Neuropeptides can coexist in same nerve terminals with classic transmitters. What causes their release?

A

LARGE amounts of Ca (They are not released at active zones since the vesicles are too large to fit into the docking complex)

123
Q

What type of neurotransmitter are opioids?

A

Neuropeptide

124
Q

What type of neurotransmitter are vassopressin and oxytocin?

A

Neuropeptides

125
Q

What are the three endogenous opioid families?

A

Endorphins
Enkephalins
Dynorphins

126
Q

What is the one gaseous neurotransmitter?

A

NO

127
Q

How is NO produced?

A

by the action of the enzyme nitric oxide synthase

128
Q

How NO synthase regulated?

A

The enzyme is regulated by Ca++ binding to the Ca++ sensor protein calmodulin.

129
Q

True or false: NO is contain in synaptic vesicles

A

False- it is released as soon as it is made to affect nearby cells

130
Q

What class of neurotransmitter are ananamide and 2-arachidonylglycerol?

A

Endocannaboids

131
Q

How are endocannaboids produced?

A

Via enzymatic degradation of membrane lipids

132
Q

What are the two types of endocannaboid receptors?

A

CB1 and CB2

133
Q

What does THC bind to?

A

CB1 and CB2