Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Parasympathetic = acetylcholine
Sympathetic = noradrenaline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the structure of acteylcholine?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the structure of noradrenaline?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is suxamethonium?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is citalopram?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is neostigmine?

A

Is an acethycholinesterase inhibitor, this increases neurotransmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
What amino acids act as an inhibitory NT in the CNS? What is their common structure?
GABA Glycine Both contain carboxyl and primary amine group, no other functional groups
25
What other substances may influence CNS neurotransmission?
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)
26
What is an example of an amine (not a monoamine) that is a NT?
Acetycholine
27
What are monoamines? What are some examples of NT in the CNS that are monoamines?
Have a single amine group in its structure connected to an aromatic ring by a two chain carbon. Seratonin etc
28
What are the different categories of monoamines and what are they derived from?
Indolamines - d from trytophan Imidazolamines - d from histidine Catecholamines - d from tyrosine
29
Give examples of indolamines NT
Melatonin Seratonin
30
Give example of imidazolamines NT
Histamine
31
Give example of catecholamines NT
Dopamine and noradrenaline
32
Give an overview of GABA.
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
What is the function and structure of GABA A(subscript) receptors?
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
What is the clinical relevance of GABA?
Used as an aneasthestic To treat epilepsy To treat anxiety and insomnia
35
What is meant by modulatory neurotransmission?
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
What are some of the functions of dopamine pathways?
Reward Pleasure Fine tuning motor functioning (basal ganglia) Compulsion Preservation
37
Dopamine -classification -receptors -signal transduction -function
Modulatory NT D1-D5 GPCRs Intiates and execute movement (basal ganglia) EMotions and organisation of thought (limbic system) Inhibition of prolactin
38
Norephinephrine -classification -receptors -signal transduction -function
Modulatory NT Adrenergic receptors GPCRs Behavioural arousal and level of awareness
39
Seratonin -classification -receptors -signal transduction -function
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
Acetylcholine -classification -receptors -signal transduction -function
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
Glutamate -classification -receptors -signal transduction -function
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
What does ionotropic and metabotropic receptor meaning?
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
GABA -classification -receptors -signal transduction -function
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
Glycine -classification -receptors -signal transduction -function
Is an inhibitory NT Binds to glycine receptors Ligand gated ion channels INhibits motor control in the spinal cord
45
What adisorders are associated with dopamine?
Parkinsons disease Shizophrenia and affective disorders
46
What disorders is noradrenaline associated with ?
Depression, anxiety and panic disorders.
47
What disorders are associated with Seratonin?
Depression Emesis (vommitting)
48
What disorders is acetylcholine associated with?
Alzheimer disease Amyotrophic lateral sclerosis Huntington disease
49
What disorders are associated with glutamate?
Epilepsy and schizophrenia
50
What disorders are associated with GABA?
Huntington disease
51
What are the different types of depression?
Major Depressive Disorder (17% lifetime prevelance) Mixed anxiety and depressive disorder Bipolar affective disorder (1-2% lifetime prevalence)
52
What is the monoamine hypothesis of depression?
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
What is important to note about the function of noradrenaline?
Can be exictatory or inhibitory in action
54
What are some of the roles of seratonin?
Gut motility Mood Hallucinations and behvaiour Sleep/wakefullness
55
What are some of the roles regulated by noradrenaline?
Blood pressure reulation Mood
56
What is some of the evidence supporting the monoamine hypothesis of depression?
That clinical effects of drugs that alleviate of cause the symptoms of depression and their known neurochemical effects on monoaminergic transmission.
57
What drugs can increase mood in depressed patients? How?
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
What drugs and treatment decrease/worsen mood in depressive patients? How?
Reserpine - Inhibits noradrenaline and 5 HT synthesis alpha-methyltyrosine - inhibits noradrenaline synthesis Methyldopa - inhibits noradrenaline synthesis
59
What pharmacologically can cause a relpase in SSRI treated depression patiens?
Tryptophan depletion Causes a decrease in 5-HT syntehsis
60
What are monoamine oxidases? What are the difference types?
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
What are monoamine transporters? What are the different types?
Are functional plasma proteins that help regulate the extracellular level of monoamine neurotransmitter. SERT - seratonin reuptake transporter NET - noradrenaline reuptake DAT - dopamine reabsorber
62
What are some of the potential targets for antidepressant drugs action in the noradrenergic and sertonergic neurotransmission?
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
What is dangerous about the immediate effects of antidepressant pharmacological treatment?
Increased potential for agitation, anxiety and suicidal agitation
64
What is amitripytyline (anti-depressant drug), why is it described as dirty pharmacology?
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
What is the proposed mechanism for how anti-depressants work?
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
What is tyramine with MAOI 'the cheese effect'?
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
What is the evidence against the monoamine hypothesis?
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
What are some examples of BNF approved Tricyclic Antidepressants (TCA)?
Amitriptyline Nortriptyline
69
What are some examples of BNF approaved SSRIs?
Fluoxetine Citalopram
70
What are some examples of BNF approved SNRIs?
Venlafaxine Duloxetine
71
What are some examples of BNF approved MAOIs?
Phenelzine Moclobemide
72
What is an example of an atypical antidepressant and how does it work?
Mirtazapine Is an antagonist of alpha 2 adrenoceptors and 5HT2 receptors. increase noradrenaline release into the synapse
73
What is tetanic fade?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions