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Neuro (not zara) > 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 is a drug?

A

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

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3
Q

What 3 questions should we ask when considering the pharmacology of a drug?

A

1) What is the target for the drug?
2) Where is the effect produced
3) What is the response produced after interaction with this target?

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4
Q

What are the four most common drug targets?

A

Receptors, Enzymes, Transport Proteins and Ion channels

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5
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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6
Q

What is an adverse affect?

A

A side effect which has negative health consequences

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7
Q

What is a side effect?

A

An effect produced by the drug that is secondary to the intended effect

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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 are off target side effects?

A

Side effects that have effects on parts of the body that arent the target site

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10
Q

What are on target side effects?

A

Side effects that have effects on target part of body but on different tissue

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11
Q

Which kind of side effect increases as dosage of a drug increases? Off target or on target

A

Off target

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12
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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13
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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14
Q

Describe the two effects that drugs can have on their target

A

-Enhance activation of target
-Reduce/prevent activation of target

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15
Q

What targets do atorvastatin, amlodipine, salbutamol and citalopram have?

A
  • Atorvastatin → enzyme
  • Citalopram → transport protein
  • Salbutamol → receptor
  • Amlodipine → ion channel
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16
Q

What is the size range of the synaptic cleft?

A

20-100nm

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17
Q

What is the purpose of spines being present on the surface of dendrites?

A

They contain protein molecules that increase the surface area for information reception

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18
Q

What type of transmission if an action potential?

A

Electrical transmission

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19
Q

What type of transmission is synaptic transmission?

A

Chemical transmission

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20
Q

What are the 4 characteristics of synaptic transmission?

A
  • Rapid timescale
  • Diversity
  • Plasticity
  • Learning and memory
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21
Q

What are some amino acid NT’s?

A

Glutamate, GABA and glycine

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22
Q

Which amino acid NTs are inhibitory?

A

GABA and glycine

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23
Q

Which amino acid NTs are excitatory?

A

Glutamate

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24
Q

What are some amine neurotransmitters?

A

Noradrenaline, adrenaline and dopamine

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25
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

26
Q

What are the 2 methods by which the NT can be inactivated after depolarising the post-synaptic terminal

A
  • Reuptake of NT via protein transport channel where it is reloaded into synaptic vesicles
  • Enzymatic degradation within the synaptic cleft
27
Q

What are vesicular proteins targets for?

A

Neurotoxins

28
Q

What is an example of a neurotoxin?

A

Botulinum toxin

29
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

30
Q

What does botulinum cause?

A

Flaccid paralysis due to complete muscle relaxation

31
Q

Give a use of botulinum toxin in plastic surgery

A

Botox - causes smoothing of brow as muscle becomes flaccid

32
Q

What is alpha latrotoxin?

A

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

33
Q

What is the effect of Zn2+ dependant endopeptidases?

A

They inhibit transmitter release

34
Q

What is an example of a Zn2+ dependant endopeptidases?

A

Tetanus toxin C tetani

35
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

36
Q

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

A

Fast response

37
Q

What are some examples of ion channel linked receptors?

A

glutamate, GABA and glycine receptors

38
Q

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

A

Slow

39
Q

How do G protein linked receptors work?

A

NT binding causes binding of receptor to G protein which binds to effector

40
Q

What are some examples of G Coupled Protein receptors?

A

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

41
Q

What are the two types of Glutamate receptors?

A

NMDA receptors
AMPA receptors

42
Q

Which ions are NMDA receptors permeable to?

A

Na+ and Ca+

43
Q

Which ions are AMPA receptors permeable to?

A

Na+

44
Q

Where are AMPA receptors found?

A

In the majority of fast excitatory synapses

45
Q

Outline the process that occurs at an excitatory glutamate synapse

A

1) Glutamate synthesised from glucose via TCA cycle and transamination in presynaptic terminal
2) Loaded into vesicles, AP comes, depolarises membrane, Ca2+ influx, stimulates exocytotic release of Glu into synaptic cleft, Glu diffuses across
3) Glu reversibly binds to postsynaptic receptors linked to ion channels (AMPA and NMDA) which produces response
4) Glu inactivated by reuptake into presynaptic nerve terminal to be reused or by glutamine-glutamate cycle

46
Q

What is the glutamine-glutamate cycle?

A

1) After synaptic transmission, glutamate is rapidly taken up by glial cells via excitatory amino acid transporters on their surface
2) In the glial cell, glutamate is converted to glutamine by glutamine synthetase
3) Glutamine is released from the glial cell and is pumped back into the presynaptic terminal to be recycled into glutamate

47
Q

What does an EEG (electroencephalography) measure

A

Electrical activity in the brain

48
Q

What happens to neurones firing patterns during a seizure?

A

they begin firing in an abnormal, excessive and synchronised manner

49
Q

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

A

GABA receptors or K+ channels

50
Q

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

A

Glutamate

51
Q

Draw an gluatmate and glutamine curve

A

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

52
Q

Outline the process that occurs at an inhibitory GABA-A receptors

A

1) GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD) in presynaptic terminal
2) AP comes, depolarises membrane, Ca2+ influx, exocytosis of GABA into synaptic cleft, diffusion across cleft
3) GABA reversibly binds to post-synaptic GABA-A receptors (linked to Cl- ion channels, Cl- influx into postsynaptic cell, hyperpolarisation) → this is inhibitory effect
4) Rapid uptake of GABA by GABA transporters (GATs) into presynaptic terminal to be reused
5) OR GABA taken up by glial cells and modified by GABA-transaminase (GABA-T) to succinic semialdehyde

53
Q

Which drugs facilitate GABA transmission?

A

Anti-epileptic
Anxiolytic
Sedative
Muscle relaxants

54
Q

What is the shape of the GABA receptor and why is it useful?

A

Pentameric because there are lots of binding sites for different drugs

55
Q

What is the drug target for diazepam?

A

The GABA receptor

56
Q

How does Diazepam work?

A

Binds to the GABA receptor and increases the effectiveness of GABA activation, meaning an action potential is less likely to fire, therefore decrease seizure symptoms

57
Q

What is a febrile seizure?

A

A convulsions when a child has a fever over 38*

58
Q

How does Lamotrigine work as an ant-epileptic medication?

A
  • Binds to and blocks voltage gated sodium channels on glutamatergic neurones in temporal lobe
  • This reduces neuronal depolarisation which would lead to glutamate NT release- so this is decreased and there is less excitatory stimulation of the post-synaptic neurone
59
Q

How does pregabalin work?

A

Blocks Ca2+ ion channels meaning less Ca2+ influx and so less glutamate released and therefore less excitatory stimulation of the post synaptic neurones

60
Q

How does levetiracetam work?

A

Binds to synaptic vesicle protein SV2A in glutamatergic neurones in the temporal lobe and interferes with vesicles fusion and reduces exocytosis of glutamate this decreasing excitatory activation of the post synaptic neurone

Neuro (not zara) (10 decks)

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