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Unit 6 Neurology > Neurotransmitters And Neuropharmacology > Flashcards

Neurotransmitters And Neuropharmacology Flashcards

1
Q

What is the typically neurotransmitter released between the pre and post synaptic neurones?

A

Acetylcholine

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2
Q

What neurotransmitter is typically released from paraympathetic and sympathetic neurones at the effector site?

A

Parasympathetic = acetylcholine
Sympathetic = noradrenaline.

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3
Q

What is the structure of acteylcholine?

A
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4
Q

What is the structure of noradrenaline?

A
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5
Q

What classification of neurotransmitter is noradrenaline?
What other neurotransmitters are part of this classifcation?

A

A cathecholamine
Others examples are dopamine and adrenaline

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5
Q

What classification of neurotransmitter is noradrenaline?
What other neurotransmitters are part of this classifcation?

A

A cathecholamine
Others examples are dopamine and adrenaline

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6
Q

Why is the effect of drugs affecting synapses difficult to predict?

A

Due to the complexity and sheer volume of synapses, that interact in different ways throught the PNS and the CNS.

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7
Q

What is the mechanism of neurotransmission at a synapse in the CNS/PNS?

A

NT is synthesised and stored in vesicles.
An action potential arrives at the presynaptic terminal, this depolarisation causes the opening of calcium ion channels.
The influx of Ca2+ causes vesicles to fuse with the presynaptic membrane.
NT is released into the synaptic cleft by exocytosis and crosses the cleft by diffusion.
NT binds to receptors on the post synaptic membrane.
This causes opening of closing of voltage gated ion channels.
The excitatory/inhibitory postsynaptic potential changes the excitability of the cell.
NT is removed by degrading enzyme or reuptaked by glial cells.
Vesicles are reconstructed

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8
Q

What different sites/stages may be used by drugs trying to cause activation at a synapse?

A

Increase the amount of precursor for the NT
Induce NT release and difussion
Postsynaptic receptor antagonist
Inhibit NT reuptake
Inhibit NT breakdown

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9
Q

What is L-DOPA?

A

A pro-drug, used in the last line treatment to parkinsons disease.
Crosses the blood brain barrier, is decarboxylated to form dopamine
Hence L-DOPA acts as a pre-cursor for excitatory NT

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10
Q

What is alpha-latrotoxin?

A

Is found in black widow spider venom.
Promotes calcium ion reflux into the presynaptic membrane
This causes uncontrolled NT release.
Can cause muscle spasms, pain and rigidity.

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11
Q

What is suxamethonium?

A

Acts as an acetylcholine agonist, binds to nicotinic acetylcholine receptors (NAChR) causing depolarisation of the post synaptic membrane.

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12
Q

What is atracurium?

A

Is a non depolarising meuromuscular blocker
Binds to nicotinic receptors but does not cause the opening of voltage gated sodium ion channels (is an antagonist)

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13
Q

What is the mechanism of action of a presynaptic receptor antagonist?

A

Prevents NT release from the presynaptic neuron,
Will decrease tetanic fade.

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14
Q

What is citalopram?

A

Is an SSRI, prevents seratonin uptake, increases action potential generation at the post synaptic end plate.

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15
Q

What is neostigmine?

A

Is an acethycholinesterase inhibitor, this increases neurotransmission

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16
Q

What are the different pathways/methods of inhibiting a neurotransmission pharmacologically?

A

Disrupt the vesicle storage
Prevent vesicle fusion
Postsynaptic receptor antagonist
Ihibitis synthesis of NT
Presynaptic receptor agonist

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17
Q

What is clondine?

A

A presynaptic receptor agonist.
Binds to alpha 2 adrenoceptors, inhibits the release of noradrenaline.
These pre-synaptic α₂ receptors are coupled to Gi. The action of the agonist (NA) here will cause a reduction in cAMP and this will reduce calcium channel activity, leading to a reduction in neurotransmitter release. The βγ subunits of these G proteins also open K⁺ channels and this tends to stabilize the pre-synaptic membrane, leading to less release. So, altogether, in this case, pre-synaptic receptor activation leads to reduced neurotransmitter release and is therefore inhibitory
This has a sympatholytic effect (suppresses the sympathetic nervous system)

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18
Q

What is the effect of a presynaptic receptor antagonist?

A

Atracurium (and other non-depolarizing neuromuscular blockers) acts primarily as a competitive antagonist on the post-synaptic membrane, thereby preventing ACh from stimulating muscle contraction.
However, one of the effects is that at concentrations of drug that are too low to inhibit muscle fibre contraction from a single action potential can still cause a reduction in repetitive contractions that would normally generate muscular tetanus. It is thought that the reason synapses can continue to drive muscle contraction over time is that the released ACh also acts on pre-synaptic nicotinic (N) receptors and this causes stored vesicles to be moved to a location immediately next to the membrane ready for release. It’s a bit like moving a bullet from a magazine into the barrel!
The antagonist prevents this hence inhibits neurotransmitter release.

So, if you inhibit this receptor, you tend to slow down the ‘loading’ of the vesicles, as a result of which, tetanic contraction, which depends on continuous release of vesicles fades rapidly

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19
Q

What is fenclonine?

A

Inhibits tryptophan hydroxylase, this enzyme is essential to seratonin production. Hence inhibiting it causes a reduction in seratonin levels.

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20
Q

What is reserpine?

A

Inhibits VMAT, this is responsibel for the uptake of cytosolic monoamines into vesciles, hence when it is inhibited less seratonin, noradrenaline and dopamine are loaded into vesciles within the presynaptic membrane. So can not be transported for release.

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21
Q

What is botulinium toxin?

A

Produced by certain bacteria
Causes flaccid weakness, often causes cardiac or respiratory failure.
Cleaves SNAP-25 from the presynaptic membrane, prevents NT release from vesicle

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22
Q

What is atropine?

A

Binds to and inhibits muscalurininc acetylcholine receptors, this prevents the opening of voltage gated sodium ion channels so an action potential at the motor end plate is not generated

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23
Q

What amino acids can act as an excitatory NT in the CNS?
What is their common structure?

A

Glutamate
Aspartate
All consists of a primary amine and an carboxyl group seperated by one additional tertiary C in the carbon chain. 2-amino…….oic acid. And one oxidised carboxyl group.

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24
Q

What amino acids act as an inhibitory NT in the CNS?
What is their common structure?

A

GABA
Glycine
Both contain carboxyl and primary amine group, no other functional groups

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25
Q

What other substances may influence CNS neurotransmission?

A

Lipids - prostaglandins and endocannabinoids (inhibitory activity)
Purines - inhibit excitatory synapses
Amine *
Peptides - opioids (inhibit NT release) and tachykinins (NT to regulate gut function)
Gases - NO (EDGF) and CO (prolongs action potential, causes headaches etc)

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26
Q

What is an example of an amine (not a monoamine) that is a NT?

A

Acetycholine

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27
Q

What are monoamines?
What are some examples of NT in the CNS that are monoamines?

A

Have a single amine group in its structure connected to an aromatic ring by a two chain carbon.
Seratonin etc

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28
Q

What are the different categories of monoamines and what are they derived from?

A

Indolamines - d from trytophan
Imidazolamines - d from histidine
Catecholamines - d from tyrosine

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29
Q

Give examples of indolamines NT

A

Melatonin
Seratonin

30
Q

Give example of imidazolamines NT

A

Histamine

31
Q

Give example of catecholamines NT

A

Dopamine and noradrenaline

32
Q

Give an overview of GABA.

A

Full name y-aminobutyric acid
Is the primary inhibitory NT in the brain
Reduces post-synpatic excitability and suppresses neuronal activity
Binds to GABA A (subscript) receptors.

33
Q

What is the function and structure of GABA A(subscript) receptors?

A

Bound to by GABA, hence is a ligand gated ion channel
Cys-loop family of pentamers
When activated it opens and allows the passage of chloride ions into the post synaptic membrane, this hyperpolarises the membrane making an action potential less likley.

34
Q

What is the clinical relevance of GABA?

A

Used as an aneasthestic
To treat epilepsy
To treat anxiety and insomnia

35
Q

What is meant by modulatory neurotransmission?

A

Neurotransmitters that can influence the effectiveness of other NTs.
Often release from a discrete set of neurons into the brain or into the extracellular fluid to act on neurons far away. Includes dopamine, noradrenaline, acetylcholine and seratonin.

36
Q

What are some of the functions of dopamine pathways?

A

Reward
Pleasure
Fine tuning motor functioning (basal ganglia)
Compulsion
Preservation

37
Q

Dopamine
-classification
-receptors
-signal transduction
-function

A

Modulatory NT
D1-D5
GPCRs
Intiates and execute movement (basal ganglia)
EMotions and organisation of thought (limbic system)
Inhibition of prolactin

38
Q

Norephinephrine
-classification
-receptors
-signal transduction
-function

A

Modulatory NT
Adrenergic receptors
GPCRs
Behavioural arousal and level of awareness

39
Q

Seratonin
-classification
-receptors
-signal transduction
-function

A

Modulatory NT
5HT-1 to 5HT-7
GPCRs expect 3 which is ligand gated ion channel
Ascending role: sleep, mood and mental illness, descending role:modulates pain

40
Q

Acetylcholine
-classification
-receptors
-signal transduction
-function

A

Modulatory NT
95% are muscularininc but some are nitotininc
Muscu are GPCR
Nicitoninc are ligand gated ion channels
Found primarily in internuerons (connect to brain regions)

41
Q

Glutamate
-classification
-receptors
-signal transduction
-function

A

Is an excitatory NT
Ionotropic glutamate receptors and metabotropic glutamate receptors
IG are ligand gated ion channels
MG are GPCRs
Is the major excitatory NT in the CNS.

42
Q

What does ionotropic and metabotropic receptor meaning?

A

Ionotropic is a pore for ions
Metabotropic receptors - activate a series of metabolic reactions or signalling pathway that may indirectly result in the opening of an ion channel

43
Q

GABA
-classification
-receptors
-signal transduction
-function

A

Is an inhibitory NT
Binds to GABA A(sub) and GABA B(sub) receptors
These are ligand gate ion channels (A) and GPCRs (B).
These regulte muscle tone, inhibit activity in the CNS and inhibit motor control in the spinal cord.

44
Q

Glycine
-classification
-receptors
-signal transduction
-function

A

Is an inhibitory NT
Binds to glycine receptors
Ligand gated ion channels
INhibits motor control in the spinal cord

45
Q

What adisorders are associated with dopamine?

A

Parkinsons disease
Shizophrenia and affective disorders

46
Q

What disorders is noradrenaline associated with ?

A

Depression, anxiety and panic disorders.

47
Q

What disorders are associated with Seratonin?

A

Depression
Emesis (vommitting)

48
Q

What disorders is acetylcholine associated with?

A

Alzheimer disease
Amyotrophic lateral sclerosis
Huntington disease

49
Q

What disorders are associated with glutamate?

A

Epilepsy and schizophrenia

50
Q

What disorders are associated with GABA?

A

Huntington disease

51
Q

What are the different types of depression?

A

Major Depressive Disorder (17% lifetime prevelance)
Mixed anxiety and depressive disorder
Bipolar affective disorder (1-2% lifetime prevalence)

52
Q

What is the monoamine hypothesis of depression?

A

The belief that the pathological cause of depression is a reduction in the level of monoamine NT in the CNS such as seratonin, Noradrenaline and dopamine.

53
Q

What is important to note about the function of noradrenaline?

A

Can be exictatory or inhibitory in action

54
Q

What are some of the roles of seratonin?

A

Gut motility
Mood
Hallucinations and behvaiour
Sleep/wakefullness

55
Q

What are some of the roles regulated by noradrenaline?

A

Blood pressure reulation
Mood

56
Q

What is some of the evidence supporting the monoamine hypothesis of depression?

A

That clinical effects of drugs that alleviate of cause the symptoms of depression and their known neurochemical effects on monoaminergic transmission.

57
Q

What drugs can increase mood in depressed patients?
How?

A

Tricyclic antidepressants - block noradrenaline and 5-HT reuptake
MAO inhibitors - increases stores of Noradrenaline and 5-HT
Electroconvulsive therapy - increase CNS responses to Noradrenaline and 5-HT
Trytophan - increases 5-HT synthesis

58
Q

What drugs and treatment decrease/worsen mood in depressive patients?
How?

A

Reserpine - Inhibits noradrenaline and 5 HT synthesis
alpha-methyltyrosine - inhibits noradrenaline synthesis
Methyldopa - inhibits noradrenaline synthesis

59
Q

What pharmacologically can cause a relpase in SSRI treated depression patiens?

A

Tryptophan depletion
Causes a decrease in 5-HT syntehsis

60
Q

What are monoamine oxidases?
What are the difference types?

A

Catalyse the breakdown of monoamines through oxidation, removing the amine grou[
MAO A preferentially acts on noradrenaline and seratonin
MAO B preferentially acts on phenyethimine
Both will act on dopamine

61
Q

What are monoamine transporters?
What are the different types?

A

Are functional plasma proteins that help regulate the extracellular level of monoamine neurotransmitter.
SERT - seratonin reuptake transporter
NET - noradrenaline reuptake
DAT - dopamine reabsorber

62
Q

What are some of the potential targets for antidepressant drugs action in the noradrenergic and sertonergic neurotransmission?

A

Inhibit monoamineoxidases in the presynaptic membrane
Inhibits a2 adrenoceptor (this inhibition will cause more 5-HT release)
Inhibit monoamine transporters (this willl increase the concentrations of monoamines in the synaptic cleft)

63
Q

What is dangerous about the immediate effects of antidepressant pharmacological treatment?

A

Increased potential for agitation, anxiety and suicidal agitation

64
Q

What is amitripytyline (anti-depressant drug), why is it described as dirty pharmacology?

A

Is a tricyclic antidepressant hence inhibits monoamine reuptake.
Has multiple effects so the phramalogical effect is difficult to infere
Has a stronger effect as an anti-muscarininc (inhibits the parasympathetic nervous system)

65
Q

What is the proposed mechanism for how anti-depressants work?

A

Pre-treatment NT are released at hypothetically low levels and areregulated by auto-inhibitory feedback loops
When intially used anti-depressants increase the duration of action potential and prevent reuptake of monoamines. However, this has a transient negative side effect of worsening depression/anxiety by inhibiting presynaptic autoreceptors, leading to less release of monoamine NT from the presynaptic membrane.
Overtime the presynaptic autoreceptors become densensitised.
The activity of the postsynaptic recepeotr in enhanced.

66
Q

What is tyramine with MAOI ‘the cheese effect’?

A

Tyramine is an amino acid found in rich foods such as cheese and alcohol.
It stimulates the release of dopamine, adrenaline and noradrenaline from vesicles.
This leads to the activation of the sympathetic nervous system.
In patients taking MAOIs these NT are not removed, this can cause a chronic increase in the sympathetic tone, leading to dangerous tachycardia and high blood pressure.

67
Q

What is the evidence against the monoamine hypothesis?

A

The therapuetic effect of antidepressants takes longer than the neurochemical reactions, suggests it is an indirect affect of changed monoamine levels rather than a direct effect.
Large variation in the effectiveness of anti-depressant drugs based on both the drug itself and different drugs in the same people.
2022 paper - there is no consistent evidence that a lack of serotonin causes depression.

68
Q

What are some examples of BNF approved Tricyclic Antidepressants (TCA)?

A

Amitriptyline
Nortriptyline

69
Q

What are some examples of BNF approaved SSRIs?

A

Fluoxetine
Citalopram

70
Q

What are some examples of BNF approved SNRIs?

A

Venlafaxine
Duloxetine

71
Q

What are some examples of BNF approved MAOIs?

A

Phenelzine
Moclobemide

72
Q

What is an example of an atypical antidepressant and how does it work?

A

Mirtazapine
Is an antagonist of alpha 2 adrenoceptors and 5HT2 receptors.
increase noradrenaline release into the synapse

73
Q

What is tetanic fade?

A

Preventing muscular tetanus
AKA decreasing the strength of continous or secondary muscle contraction caused by rapid firing of action potentials.

Unit 6 Neurology (17 decks)

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