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Bioregulatory systems > 1a Pharmacology and Neurotransmitters > Flashcards

1a Pharmacology and Neurotransmitters Flashcards

1
Q

What is the definition of pharmacology?

A

The study of how chemical agents can influence the function of living systems

a chemical substance that interacts with a specific target within a biological system to produce a physiologic effect

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2
Q

why do people take heroin?

A

euphoria
analgesia (pain relief)
cough suppression

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3
Q

which parts of the brain produce the following responses:
analgesia, euphoria, cough suppression

A

analgesia: peri-aqueductal grey region
euphoria: ventral tegmental area
cough suppression: cough nucleus

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4
Q

what 3 qs must you know the answer to when making new drugs?

A

where is the effect produced?
what is the drug target?
what is the response produced after interraction with this target?

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5
Q

What are the four most common drug targets?

A

Receptors, Enzymes, Transport Proteins and Ion channels

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6
Q

What must a successful drug show?

A

high levels of specificity for a particular target - this is to prevent the drug binding to different things and causing undesired effects

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7
Q

What is an adverse affect?

A

A side effect which has negative health consequences

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8
Q

What can cause side effects?

A

When the drug results in off-target effect, or the drug acts on different targets on the same tissue

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9
Q

What is the “safest drug”

A

Where there is the largest difference between the dose required to induce the desired effect and the dose required to induce side/adverse effects

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10
Q

Why is selectivity more important for drugs than endogenous products of the body?

A

Endogenous products are produced specifically where they act, where as drugs have to travel in the blood stream to reach their target - more chance of the drug binding to the wrong thing and causing adverse effects

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11
Q

describe briefly transmission across a few neurones

A
  1. transmitter released from 1st cell
  2. synaptic activation of 2nd cell
  3. signal integration and signal conduction by 2nd cell
  4. signal transmitted to effectors/subsequent neurones
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12
Q

what 4 things explain why we need synaptic transmission

A

rapid timescale, diversity, plasticity, learning and memory

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13
Q
A
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14
Q
A
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15
Q

What is the size range of the synaptic cleft?

A

20-100nm

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16
Q

what comes before and after a synapse?

A

pre-synaptic nerve ending/terminal button
gap 20-100nm
postsynaptic region (dendrite or cell soma)

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17
Q

What type of transmission if an action potential?

A

Electrical transmission

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18
Q

What type of transmission is synaptic transmission?

A

Chemical transmission

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19
Q

what are the 3 basic stages of synaptic transmission?

A
  1. biosynthesis, packaging and release of neurotransmitter
  2. receptor activation
  3. inactivation
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20
Q

What ion is essential for NT release?

A

Ca2+ - bind to vesicles which allows them to fuse with pre-synaptic membrane and release NT via exocytosis into synaptic cleft

transmitter release requires aan increase in intracellulr C2+ (200 um)

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21
Q

What are some amino acid NT’s?

A

Glutamate, GABA and glycine

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22
Q

What are some amine neurotransmitters?

A

Noradrenaline and dopamine

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23
Q

what are some neuropeptides transmitters?

A

opioid peptides

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24
Q

describe briefly neurotransmitter release

A
  1. membrane depolarisation
  2. Ca2+ channels open
  3. C2+ influx
  4. vesicle fusion
  5. vesicle exocytosis
  6. transmitter release
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25
Describe the stages of NT release?
1. Action potential arrives at pre-synaptic bouton 2. AP results in the opening of Ca2+ ion channels 3. This results in a large influx of Ca2+ ions into the neurone 4. The Ca2+ ions bind to the NT vesicles and cause the vesicles to fuse with the pre-synaptic membrane 5. This releases the NT into the synaptic cleft via exocytosis 6. The NT then makes contact with the receptor allowing for the depolarisation of the other neurone due to Na+ influx 7. The NT is then enzymatically degraded or taken back up into the pre-synaptic bouton
26
where are synaptic vesicles filled with neurotransmitter docled?
in the synaptic zone
27
what do special proteins on the vesicle and presynaptic membrane do?
enable fusion and exocytosis
28
How are dendrites specially adapted to their function?
They have many spines to increase the surface area for information reception
29
What is an example of a neurotoxin?
Botulinum toxin
30
Explain how botulinum toxin acts as a neurotoxin?
the botulinum toxin cleaves the SNARE proteins on the presynaptic membrane which would normally allow the NT vesicle to fuse Therefore, the vesicle cannot fuse, and NT cannot be released
31
What are SNARE proteins?
They are specific proteins found on the pre-synaptic membrane which help the NT vesicle to fuse so the NT can then be released via exocytosis
32
What does botulinum cause?
Flaccid paralysis due to complete muscle relaxation
33
Give a use of botulinum toxin in plastic surgery
Botox - causes smoothing of brow as muscle becomes flaccid
34
What is alpha latrotoxin?
Stimulates transmitter release to depletion - this means that eventually there will no ACh, leading to muscle paralysis
35
what are transmitter release requirements?
1. calcium dependent 2. transmitter containing vesicles to be docked on the presynaptic membrane 3. protein complex formation between vesicle, membrane and cytoplasmic proteins. to enable both vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis
36
What is the effect of Zn2+ dependant endopeptidases?
They inhibit transmitter release
37
What is the speed of the response when using ion channel-linked receptors?
Fast response (msecs) mediate all fast excitatory and inhibitory transmission
38
What are some examples of ion channel linked receptors?
GluR, GABAR and GlyR nAChR
39
give examples of neurotransmitters that bind to ion-linked channel receptors
CNS: glutamate, GABA NMJ: ACh at nicotinic receptors
40
what is the speed of response with G-protein coupled receptors?
SLOW (secs/mins) due to multiple step nature effectors may be enzymes (adenyl cyclase, phospholipase C, cGMP-PDE) or channel (Ca2+ or K+) can modify this but cant modify ion channel-linked receptors
41
What is an example of an inhibitory neurotransmitter?
GABA
42
What is meant by an inhibitory neurotransmitter?
A NT which makes the post-synaptic membrane less likely to propagate an action potential
43
How does GABA work as in inhibitory neurotransmitter?
It allows an influx of Cl- ions, which makes the membrane potential more negative = hyperpolarised so less likely to reach the threshold for an action potential to fire
44
What are the two types of Glutamate receptors?
NMDA receptors AMPA receptors
45
Which ions are NMDA receptors permeable to?
Na+ and Ca+
46
Which ions are AMPA receptors permeable to?
Na+
47
Where are AMPA receptors found?
In the majority of fast excitatory synapses
48
What speed of response do G-Protein-Coupled Receptors mediate?
Slow
49
What are some examples of G Coupled Protein receptors?
Muscarinic ACh receptors, dopamine receptors, noradrenaline receptors, seratonin receptors
50
What happens to glutamate in glial cells?
It is enzymatically modified by glutamine synthetase into glutamine in glial cells
51
What happens to neurones firing patterns during a seizure?
they begin firing in an abnormal, excessive and synchronised manner
52
Following excessive depolarisation during a seizure, what facilitates the hyperpolarisation?
GABA receptors or K+ channels
53
Which neurotransmitter is present in excess in the synpase during a seizure?
Glutamate
54
Draw an gluatmate and glutamine curve
Large peak of glutatmate followed by large glutamine peak - this is because the excess glutamate is metabolised into glutamine
55
Which drugs facilitate GABA transmission?
Anti-epileptic Anxiolytic Sedative Muscle relaxants
56
What word is used to describe the shape of the GABA receptor?
Pentameric
57
What is the drug target for diazepam?
The GABA receptor
58
How does Diazepam work?
Binds to the GABA receptor and increases the effectiveness of GABA activation, therefore more CL- ion uptake which hyperpolarises the post-synaptic membrane, meaning an action potential is less likely to fire, therefore decrease seizure symtpoms
59
What is a febrile seizure?
A convulsions when a child has a fever over 38*
60
How does Lamotrigine work as an ant-epileptic medication?
Acts on voltage gated sodium channel, so less depolarisation in the neurone, and less glutamate transmission
61
How does pregabalin work?
Blocks Ca2+ ion channels meaning less Ca2+ influx which is needed to bind to NT vesicles so they can fuse with the membrane and be released - less glutamate transmission
62
How does levetiracetam work?
Interferes with vesicle fusion which reduces the exocytosis of glutamate which decreases the excitory activation of the post-synaptic neurone
63
Why should sodium valpoate not be used on females with child bearing potential?
It is teratogenic - this means it can impact the development of the foetus
64
65
what are the 3 basic stages of synaptic transmission?
1. biosynthesis, packaging and release of neurotransmitter 2. receptor activation 3. inactivation
66
what are transmitter release requirements?
1. calcium dependent 2. transmitter containing vesicles to be docked on the presynaptic membrane 3. protein complex formation between vesicle, membrane and cytoplasmic proteins. to enable both vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis

Bioregulatory systems (4 decks)

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