Neurotransmission Flashcards
(95 cards)
1
Q
What are the four main sections of the typical neuronal structure?
A
- Cell soma
- Dendrites
- Axon
- Terminals
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
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
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
5
Q
What does the post-synaptic response depend on in neurotransmission?
A
- Nature of the transmitter
- Nature of the receptor
6
Q
Give two examples of receptors found in neurotransmission
A
- Ligand-gated ion channels
- G-protein coupled receptors
7
Q
How many neurotransmitters have been identified in the CNS?
A
Over 30
8
Q
What chemical classes can the neurotransmitters in the CNS be divided into?
A
- Amino acids
- Biogenic amines
- Peptides
9
Q
Give 5 examples of biogenic amine neurotransmitters in the CNS
A
- Acetylcholine
- Noradrenaline
- Dopamine
- Serotonin
- Histamine
10
Q
Give 6 examples of peptide neurotransmitters in the CNS
A
- Dynorphin
- Enkephalins
- Substance P
- Somatostatin
- Cholecystokinin
- Neuropeptide Y
11
Q
What are the types of amino acid neurotransmitters?
A
- Excitatory amino acids
- Inhibitory amino acids
12
Q
What is the main excitatory amino acid neurotransmitter?
A
Glutamate
13
Q
What % of all CNS synapses are glutamatergic?
A
Over 70%
14
Q
Describe the distribution of glutamatergic neurotransmitters in the CNS
A
They are present throughout the CNS
15
Q
Give two inhibitory amino acid neurotransmitters
A
- GABA
- Glycine
16
Q
What are the types of glutamate receptors?
A
- Ionotrophic
- Metabotrophic
17
Q
What are the types of ionotropic glutamate receptors?
A
- AMPA receptors
- Kainate receptors
- NMDA receptors
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+
19
Q
What does activation of ionotrophic glutamate receptors cause?
A
Depolarisation, and therefore increased excitability
20
Q
What are the types of metabotrophic glutamate receptors?
A
mGluR 1-7
21
Q
What kind of receptor are the metabotrophic glutamate receptors?
A
G-protein coupled receptors
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
23
Q
What effect do excitatory neurotransmitters have on the post-synaptic cell?
A
They cause depolarisation
24
Q
How do excitatory neurotransmitters cause depolarisation of the post-synaptic cell?
A
By acting on ligand-gated ion channels
25
What is it called when excitatory neurotransmitters cause depolarisation of the post-synpatic cell?
Excitatory post-synaptic potential
26
What does depolarisation of the post-synaptic cell by excitatory neurotransmitters cause?
More action potentials
27
What kind of receptors do glutamatergic synpases have?
Both AMPA and NMDA
28
What do AMPA receptors in glutamatergic synapses mediate?
The initial fast depolarisation
29
What are NMDA receptors permeable to?
Ca2+
30
What do NMDA receptors require to allow ion flow through the channel?
Need glutamate to bind, and the cell to be depolarised
31
What acts as a co-agonist to NMDA receptors in the glutamatergic synapses?
Glycine
32
Where do glutamate receptors have an important role?
In learning and memory
33
What effect can activation of NMDA receptors and mGluRs have on AMPA receptors?
Can up-regulate them
34
What does strong, high frequency stimulation to glutamate receptors cause?
Long term potentiation
35
What is important for the induction of LTP?
Ca2+ entry through NMDA receptors
36
What does too much Ca2+ entry through NMDA receptors cause?
Excitotoxicity
37
What is the result of too much Ca2+ entry through NMDA receptors causing excitotoxicity?
Too much glutamate can cause excitotoxicity
38
What is the main inhibitory neurotransmitter in the brain?
GABA
39
Where does glycine act as an inhibitory neurotransmitter?
Mostly in the brainstem and spinal cord
40
What ion channels do GABAA and glycine receptors contain?
Integral Cl- channels
41
What does the opening of the Cl- channels in the GABAA and glycine receptors cause?
Hyperpolarisation
42
What is it called when opening the Cl- channel in GABAA and glycine receptors causes hyperpolarisation?
Inhibitory post-synaptic potential
43
What is the result of the inhibiotry post-synaptic potential produced by GABAA and glycine receptors?
There is decreased action potenital firing
44
What kind of role to GABAA G-protein coupled receptors have?
A modulatory role
45
What drugs bind to GABAA receptors?
* Barbiturates
* Benzodiazepines
46
What effect do barbiturates and benzodiazepines have when they bind to GABAA receptors?
They enhance the response to GABA
47
What are the actions of barbituates?
* Anxiolytic and sedative actions
* Sometimes used as anti-epileptic drugs
48
Why are barbiturates no longer used for their anxiolytic and sedative actions?
Because there is a risk of fatal overdose, dependance, and tolerance
49
What effects do benzodiazepines have?
Sedative and anxiolytic effects
50
What are benzodiazepines used to treat?
* Anxiety
* Insomnia
* Epilepsy
51
What neurones release glycine?
Inhibitory neurones in the spinal cord
52
What do biogenic amines mostly act as?
Neuromodulators
53
Where is ACh released as a neurotransmitter?
In the neuromuscular junction
54
Where does an ACh ganglion synapse?
In the ANS
55
Is the post-ganglionic fibre sympathetic or parasympathetic when ACh is the neurotransmitter?
Parasympathetic
56
What does ACh act on in the brain?
Both nicotinic and muscarinic receptors
57
Is ACh excitatory or inhibitory in the brain?
Mainly excitatory
58
What is often the purpose of ACh receptors on pre-synaptic terminals in the brain?
To enhance the release of other transmitters
59
Where do neurones in the cholinergic pathways in the CNS originate?
In the basal forebrain and brainstem
60
Where do the neurones originating in the basal forebrain and brainstem in the cholinergic pathways in the CNS go?
They give diffuse projections to many parts of the cortex and the hippocampus. *There are also local cholinergic interneurones*
61
Give an example of where local cholinergic interneurones are found?
In the corpus striatum
62
What are the cholinergic pathways in the CNS involved in?
* Arousal
* Learning
* Memory
* Motor control
63
How are cholinergic pathways in the CNS associated with Alzheimers disease?
Degeneration of cholinergic neurones in the nucleus basalis is associated with Alzheimers disease
64
What is used to alleviate the symptoms of Alzheimers disease?
Cholinesterase inhibitors
65
What are the dopaminergic pathways in the CNS?
* Tubero-hypophyseal pathway
* Mesocortical pathway
* Mesolimbic pathway
* Nigrostriatal pathway
66
Draw a diagram illustrating the dopaminergic pathways in the CNS
67
What is the nigrostraital pathway involved in?
Motor control
68
What are the mesocortical and mesolimbic pathways involved in?
* Mood
* Arousal
* Reward
69
What conditions are associated with dopamine dysfunction?
* Parkinson's disease
* Schizophrenia
70
What is Parkinson's disease associated with?
Loss of dopaminergic neurones
71
Which dopaminergic neurones are lost in Parkinson's disease?
Those that provide substantia nigra input to corpus striatum
72
How can Parkinson's disease be treated?
With levodopa
73
What happens to levodopa in the body?
It is converted to dopamine by DOPA decarboxylase
74
What is the theorised that schizophrenia is due to?
Too much dopamine
75
What is the evidence for schizophrenia being due to the release of too much dopamine?
* Amphetamine releases dopamine and noradrenaline, and produces schizophrenic like behaviour
* Anti-psychotic drugs are antagonists of dopamine D2 receptors
76
Draw a diagram illustrating how carbidopa therapy penetrates the blood brain barrier
77
Where does noradrenaline act as a neurotransmitter?
At postganglionic-effector synpases in the ANS
## Footnote
*Also acts as a neurotransmitter in the CNS*
78
What does noradrenaline operate through?
G-protein coupled alpha- and beta-adrenoceptors
79
How do receptors to noradrenaline in the brain differ to in the periphery?
They are the same
80
Where are the cell bodies of NA containing neurones located in the brain?
In the pons and medulla of the brainstem
81
What happens to NA after it is released from neurones in the brainstem?
There is diffuse release of NA throughout the cortex, hypothalamus, amygdala and cerebellum
82
Specificially, where does most NA in the brain come from?
A group of neurones in the locus ceruleus
83
When are locus ceruleus inactive?
During sleep
84
When does the activity of locus cereuleus neurones increase?
During behavioural arousal
85
What effect do amphetamines have on noradrenaline?
They increase the release of noradrenaline and dopamine, and increase wakefulness
86
What is the relationship between noradrenaline, and mood and state of arousal?
Depression may be associated with deficiency of NA
87
What is the distribution of serotonergic neurones similar to?
That of noradrenergic neurones
88
What are the functions of serotonergic pathways in the CNS?
* Sleep/wakefulness
* Mood
89
Where are SSRIs used?
In the treatment of depression and anxiety disorders
90
What is the monoamine theory of depression?
That depression is due to a functional deficit of monoamine transmitters in some brain areas
91
What is the monoamine theory of mania?
That mania is due to a functional excess of monoamine transmitters
92
Where are the monoamine pathways clinically important?
Many drugs used in the treatment of mood disorders act on the monoamine pathways
93
Give three drugs used in the treatment of mood disorders that act on the monoamine pathways?
* Tricyclic antidepressants
* SSRIs
* MAOIs
94
What do tricyclic antidepressants do?
Inhibit the uptake of NA/serotonin
95
What do MAOIs?
Inhibit monoamine oxidase, which is the enzyme that metabolises monoamines, to prevent the breakdown of monoamines within the terminal
