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BRS NEUROLOGY > 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

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2
Q

What are the four most common drug targets?

A

Receptors, Enzymes, Transport Proteins and Ion channels

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3
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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4
Q

What is an adverse affect?

A

A side effect which has negative health consequences

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5
Q

What can cause side effects?

A

When the drug results in same target on a different tissue, or the drug acts on different targets on the same tissue

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6
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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7
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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8
Q

What is the size range of the synaptic cleft?

A

20-100nm

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9
Q

What type of transmission is an action potential?

A

Electrical transmission

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10
Q

What type of transmission is synaptic transmission?

A

Chemical transmission

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11
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

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12
Q

What are some amino acid NT’s?

A

Glutamate, GABA and glycine

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13
Q

What are some amine neurotransmitters?

A

Noradrenaline, adrenaline and dopamine

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14
Q

Describe the stages of NT release?

A
  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
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15
Q

How are dendrites specially adapted to their function?

A

They have many spines to increase the surface area for information reception

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16
Q

What is an example of a neurotoxin?

A

Botulinum toxin

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17
Q

Explain how botulinum toxin acts as a neurotoxin?

A

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

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18
Q

What are SNARE proteins?

A

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

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19
Q

What does botulinum cause?

A

Flaccid paralysis due to complete muscle relaxation

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20
Q

Give a use of botulinum toxin in plastic surgery

A

Botox - causes smoothing of brow as muscle becomes flaccid

21
Q

What is alpha latrotoxin?

A

Stimulates transmitter release to depletion - this means that eventually there will no ACh, leading to muscle paralysis

22
Q

What is the effect of Zn2+ dependant endopeptidases?

A

They inhibit transmitter release

23
Q

What is an example of a Zn2+ dependant endopeptidases?

A

Tetanus toxin C tetani

24
Q

How does tetanus toxin C tetani work?

A

Blocks GABA release
Since GABA is an inhibitory NT, blocking it results in paralysis due to violent musclar spasms as the muscles are continually contracted

25
Q

What is the speed of the response when using ion channel-linked receptors?

A

Fast response

26
Q

What are some examples of ion channel linked receptors?

A

nAChR, GluR, GABA and GlyR

27
Q

What is an example of an inhibitory neurotransmitter?

A

GABA

28
Q

What is meant by an inhibitory neurotransmitter?

A

A NT which makes the post-synaptic membrane less likely to propagate an action potential

29
Q

How does GABA work as in inhibitory neurotransmitter?

A

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

30
Q

What are the two types of Glutamate receptors?

A

NMDA receptors
AMPA receptors

31
Q

Which ions are NMDA receptors permeable to?

A

Na+ and Ca+

32
Q

Which ions are AMPA receptors permeable to?

A

Na+

33
Q

Where are AMPA receptors found?

A

In the majority of fast excitatory synapses

34
Q

What speed of response do G-Protein-Coupled Receptors mediate?

A

Slow

35
Q

What are some examples of G Coupled Protein receptors?

A

Muscarinic ACh receptors, dopamine receptors, noradrenaline receptors, seratonin receptors

36
Q

What happens to glutamate in glial cells?

A

It is enzymatically modified by glutamine synthetase into glutamine in glial cells

37
Q

What happens to neurones firing patterns during a seizure?

A

they begin firing in an abnormal, excessive and synchronised manner

38
Q

Following excessive depolarisation during a seizure, what facilitates the hyperpolarisation?

A

GABA receptors or K+ channels

39
Q

Which neurotransmitter is present in excess in the synpase during a seizure?

A

Glutamate

40
Q

Draw an glutamate and glutamine curve

A

Large peak of glutamate followed by large glutamine peak - this is because the excess glutamate is metabolised into glutamine

41
Q

Which drugs facilitate GABA transmission?

A

Anti-epileptic
Anxiolytic
Sedative
Muscle relaxants

42
Q

What word is used to describe the shape of the GABA receptor?

A

Pentameric

43
Q

What is the drug target for diazepam?

A

The GABA receptor

44
Q

How does Diazepam work?

A

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

45
Q

What is a febrile seizure?

A

A convulsions when a child has a fever over 38*

46
Q

How does Lamotrigine work as an ant-epileptic medication?

A

Acts on voltage gated sodium channel, so less depolarisation in the neurone, and less glutamate transmission

47
Q

How does pregabaline work?

A

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

48
Q

How does levetiracetam work?

A

Interferes with vesicle fusion which reduces the exocytosis of glutamate which decreases the excitory activation of the post-synaptic neurone

49
Q

Why should sodium valpoate not be used on females with child bearing potential?

A

It is teratogenic - this means it can impact the development of the foetus

BRS NEUROLOGY (22 decks)

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