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Neurotransmission Flashcards

1
Q

What are the four main sections of the typical neuronal structure?

A
  • Cell soma
  • Dendrites
  • Axon
  • Terminals
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2
Q

What effect does depolarisation in the terminal have in neurotransmission?

A

It opens voltage-gated Ca2+ channels, and Ca2+ ions enter the terminal

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3
Q

What effect does the entrance of Ca+ ions into the terminal have in neurotransmission?

A

It causes the vesicles to fuse and release neurotransmitter

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4
Q

What happens to the neurotransmitter released from the terminal in neurotransmission?

A

It diffuses across the synaptic cleft, and binds to receptors on the post-synaptic membrane

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5
Q

What does the post-synaptic response depend on in neurotransmission?

A
  • Nature of the transmitter
  • Nature of the receptor
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6
Q

Give two examples of receptors found in neurotransmission

A
  • Ligand-gated ion channels
  • G-protein coupled receptors
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7
Q

How many neurotransmitters have been identified in the CNS?

A

Over 30

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8
Q

What chemical classes can the neurotransmitters in the CNS be divided into?

A
  • Amino acids
  • Biogenic amines
  • Peptides
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9
Q

Give 5 examples of biogenic amine neurotransmitters in the CNS

A
  • Acetylcholine
  • Noradrenaline
  • Dopamine
  • Serotonin
  • Histamine
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10
Q

Give 6 examples of peptide neurotransmitters in the CNS

A
  • Dynorphin
  • Enkephalins
  • Substance P
  • Somatostatin
  • Cholecystokinin
  • Neuropeptide Y
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11
Q

What are the types of amino acid neurotransmitters?

A
  • Excitatory amino acids
  • Inhibitory amino acids
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12
Q

What is the main excitatory amino acid neurotransmitter?

A

Glutamate

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13
Q

What % of all CNS synapses are glutamatergic?

A

Over 70%

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14
Q

Describe the distribution of glutamatergic neurotransmitters in the CNS

A

They are present throughout the CNS

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15
Q

Give two inhibitory amino acid neurotransmitters

A
  • GABA
  • Glycine
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16
Q

What are the types of glutamate receptors?

A
  • Ionotrophic
  • Metabotrophic
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17
Q

What are the types of ionotropic glutamate receptors?

A
  • AMPA receptors
  • Kainate receptors
  • NMDA receptors
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18
Q

Describe a ionotrophic glutamate receptor

A

It is an ion channel that is permeable to Na+ and K+, and in some cases Ca2+

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19
Q

What does activation of ionotrophic glutamate receptors cause?

A

Depolarisation, and therefore increased excitability

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20
Q

What are the types of metabotrophic glutamate receptors?

A

mGluR 1-7

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21
Q

What kind of receptor are the metabotrophic glutamate receptors?

A

G-protein coupled receptors

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22
Q

What does activation of metabotrophic glutamate receptors lead to?

A

Either;

  • Changes in IP3 and Ca2+ metabolism
  • Inhibition of adenylate cyclase, and decreased cAMP levels
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23
Q

What effect do excitatory neurotransmitters have on the post-synaptic cell?

A

They cause depolarisation

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24
Q

How do excitatory neurotransmitters cause depolarisation of the post-synaptic cell?

A

By acting on ligand-gated ion channels

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25
Q

What is it called when excitatory neurotransmitters cause depolarisation of the post-synpatic cell?

A

Excitatory post-synaptic potential

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26
Q

What does depolarisation of the post-synaptic cell by excitatory neurotransmitters cause?

A

More action potentials

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27
Q

What kind of receptors do glutamatergic synpases have?

A

Both AMPA and NMDA

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28
Q

What do AMPA receptors in glutamatergic synapses mediate?

A

The initial fast depolarisation

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29
Q

What are NMDA receptors permeable to?

A

Ca2+

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30
Q

What do NMDA receptors require to allow ion flow through the channel?

A

Need glutamate to bind, and the cell to be depolarised

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31
Q

What acts as a co-agonist to NMDA receptors in the glutamatergic synapses?

A

Glycine

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32
Q

Where do glutamate receptors have an important role?

A

In learning and memory

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33
Q

What effect can activation of NMDA receptors and mGluRs have on AMPA receptors?

A

Can up-regulate them

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34
Q

What does strong, high frequency stimulation to glutamate receptors cause?

A

Long term potentiation

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35
Q

What is important for the induction of LTP?

A

Ca2+ entry through NMDA receptors

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36
Q

What does too much Ca2+ entry through NMDA receptors cause?

A

Excitotoxicity

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37
Q

What is the result of too much Ca2+ entry through NMDA receptors causing excitotoxicity?

A

Too much glutamate can cause excitotoxicity

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38
Q

What is the main inhibitory neurotransmitter in the brain?

A

GABA

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39
Q

Where does glycine act as an inhibitory neurotransmitter?

A

Mostly in the brainstem and spinal cord

40
Q

What ion channels do GABAA and glycine receptors contain?

A

Integral Cl- channels

41
Q

What does the opening of the Cl- channels in the GABAA and glycine receptors cause?

A

Hyperpolarisation

42
Q

What is it called when opening the Cl- channel in GABAA and glycine receptors causes hyperpolarisation?

A

Inhibitory post-synaptic potential

43
Q

What is the result of the inhibiotry post-synaptic potential produced by GABAA and glycine receptors?

A

There is decreased action potenital firing

44
Q

What kind of role to GABAA G-protein coupled receptors have?

A

A modulatory role

45
Q

What drugs bind to GABAA receptors?

A
  • Barbiturates
  • Benzodiazepines
46
Q

What effect do barbiturates and benzodiazepines have when they bind to GABAA receptors?

A

They enhance the response to GABA

47
Q

What are the actions of barbituates?

A
  • Anxiolytic and sedative actions
  • Sometimes used as anti-epileptic drugs
48
Q

Why are barbiturates no longer used for their anxiolytic and sedative actions?

A

Because there is a risk of fatal overdose, dependance, and tolerance

49
Q

What effects do benzodiazepines have?

A

Sedative and anxiolytic effects

50
Q

What are benzodiazepines used to treat?

A
  • Anxiety
  • Insomnia
  • Epilepsy
51
Q

What neurones release glycine?

A

Inhibitory neurones in the spinal cord

52
Q

What do biogenic amines mostly act as?

A

Neuromodulators

53
Q

Where is ACh released as a neurotransmitter?

A

In the neuromuscular junction

54
Q

Where does an ACh ganglion synapse?

A

In the ANS

55
Q

Is the post-ganglionic fibre sympathetic or parasympathetic when ACh is the neurotransmitter?

A

Parasympathetic

56
Q

What does ACh act on in the brain?

A

Both nicotinic and muscarinic receptors

57
Q

Is ACh excitatory or inhibitory in the brain?

A

Mainly excitatory

58
Q

What is often the purpose of ACh receptors on pre-synaptic terminals in the brain?

A

To enhance the release of other transmitters

59
Q

Where do neurones in the cholinergic pathways in the CNS originate?

A

In the basal forebrain and brainstem

60
Q

Where do the neurones originating in the basal forebrain and brainstem in the cholinergic pathways in the CNS go?

A

They give diffuse projections to many parts of the cortex and the hippocampus. There are also local cholinergic interneurones

61
Q

Give an example of where local cholinergic interneurones are found?

A

In the corpus striatum

62
Q

What are the cholinergic pathways in the CNS involved in?

A
  • Arousal
  • Learning
  • Memory
  • Motor control
63
Q

How are cholinergic pathways in the CNS associated with Alzheimers disease?

A

Degeneration of cholinergic neurones in the nucleus basalis is associated with Alzheimers disease

64
Q

What is used to alleviate the symptoms of Alzheimers disease?

A

Cholinesterase inhibitors

65
Q

What are the dopaminergic pathways in the CNS?

A
  • Tubero-hypophyseal pathway
  • Mesocortical pathway
  • Mesolimbic pathway
  • Nigrostriatal pathway
66
Q

Draw a diagram illustrating the dopaminergic pathways in the CNS

67
Q

What is the nigrostraital pathway involved in?

A

Motor control

68
Q

What are the mesocortical and mesolimbic pathways involved in?

A
  • Mood
  • Arousal
  • Reward
69
Q

What conditions are associated with dopamine dysfunction?

A
  • Parkinson’s disease
  • Schizophrenia
70
Q

What is Parkinson’s disease associated with?

A

Loss of dopaminergic neurones

71
Q

Which dopaminergic neurones are lost in Parkinson’s disease?

A

Those that provide substantia nigra input to corpus striatum

72
Q

How can Parkinson’s disease be treated?

A

With levodopa

73
Q

What happens to levodopa in the body?

A

It is converted to dopamine by DOPA decarboxylase

74
Q

What is the theorised that schizophrenia is due to?

A

Too much dopamine

75
Q

What is the evidence for schizophrenia being due to the release of too much dopamine?

A
  • Amphetamine releases dopamine and noradrenaline, and produces schizophrenic like behaviour
  • Anti-psychotic drugs are antagonists of dopamine D2 receptors
76
Q

Draw a diagram illustrating how carbidopa therapy penetrates the blood brain barrier

77
Q

Where does noradrenaline act as a neurotransmitter?

A

At postganglionic-effector synpases in the ANS

Also acts as a neurotransmitter in the CNS

78
Q

What does noradrenaline operate through?

A

G-protein coupled alpha- and beta-adrenoceptors

79
Q

How do receptors to noradrenaline in the brain differ to in the periphery?

A

They are the same

80
Q

Where are the cell bodies of NA containing neurones located in the brain?

A

In the pons and medulla of the brainstem

81
Q

What happens to NA after it is released from neurones in the brainstem?

A

There is diffuse release of NA throughout the cortex, hypothalamus, amygdala and cerebellum

82
Q

Specificially, where does most NA in the brain come from?

A

A group of neurones in the locus ceruleus

83
Q

When are locus ceruleus inactive?

A

During sleep

84
Q

When does the activity of locus cereuleus neurones increase?

A

During behavioural arousal

85
Q

What effect do amphetamines have on noradrenaline?

A

They increase the release of noradrenaline and dopamine, and increase wakefulness

86
Q

What is the relationship between noradrenaline, and mood and state of arousal?

A

Depression may be associated with deficiency of NA

87
Q

What is the distribution of serotonergic neurones similar to?

A

That of noradrenergic neurones

88
Q

What are the functions of serotonergic pathways in the CNS?

A
  • Sleep/wakefulness
  • Mood
89
Q

Where are SSRIs used?

A

In the treatment of depression and anxiety disorders

90
Q

What is the monoamine theory of depression?

A

That depression is due to a functional deficit of monoamine transmitters in some brain areas

91
Q

What is the monoamine theory of mania?

A

That mania is due to a functional excess of monoamine transmitters

92
Q

Where are the monoamine pathways clinically important?

A

Many drugs used in the treatment of mood disorders act on the monoamine pathways

93
Q

Give three drugs used in the treatment of mood disorders that act on the monoamine pathways?

A
  • Tricyclic antidepressants
  • SSRIs
  • MAOIs
94
Q

What do tricyclic antidepressants do?

A

Inhibit the uptake of NA/serotonin

95
Q

What do MAOIs?

A

Inhibit monoamine oxidase, which is the enzyme that metabolises monoamines, to prevent the breakdown of monoamines within the terminal

SO-Nervous System (18 decks)

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