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nervous system > Applied Neuro-pharmacology > Flashcards

Applied Neuro-pharmacology Flashcards

1
Q

Describe the sequence of events in synaptic transmission?

A
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2
Q

What are the different receptor types for neurotransmitters?

A

Ionotropic (respond to ligand binding)

Metabotropic (acts through a second messenger. It may be located at the surface of the cell or in vesicles)

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3
Q

Is acetylcholine uptaked into glia/neural cells or is it inactivated by breakdown?

A

Inactivated by enzymatic breakdown in the synaptic cleft

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4
Q

What are some methods of pharmacological manipulation to reduce synaptic transmission?

A

Inhibit synthesis and packaging of neurotransmitter

Activate presynaptic inhibitory receptors

Block postsynaptic receptors (such as competitive antagonists or non-competitive antagonists)

Block voltage gated calcium channels

Increase breakdown of transmitter

Block release machinery

Increase uptake of transmitter

Block voltage-gated sodium channels

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5
Q

What are some methods of pharmacological manipulation to increase synaptic transmission?

A

Increase synthesis and packaging of neurotransmitter (by increasing availability of precursors)

Activate postsynaptic receptors with an agonist

Potentiate effects of transmitter on receptor (ie increase channel open time)

Block breakdown of transmitter

Block uptake of transmitter

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6
Q

What are examples of different neurotransmitters?

A
  • Acetylcholine
  • Monoamines
    • Noradrenaline
    • Dopamine
    • Serotonin (5-HT)
  • Amino acids
    • Glutamate
    • GABA
    • Glycine
  • Purines
    • ATP
    • Adenosine
  • Neuropeptides
    • Endorphins
    • CCK
    • Substance P
  • NO
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7
Q

What are examples of monoamines that act as neurotransmitters?

A
  • Noradrenaline
  • Dopamine
  • Serotonin (5-HT)
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8
Q

What does 5-HT stand for?

A

Serotonin

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9
Q

What are examples of amino acids that act as neurotransmitters?

A
  • Glutamate
  • GABA
  • Glycine
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10
Q

What are examples of purines that act as neurotransmitters?

A
  • ATP
  • Adenosine
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11
Q

What are examples of neuropeptides that act as neurotransmitters?

A
  • Endorphins
  • CCK
  • Substance P
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12
Q

A limited range of neurotransmitters means what in terms of function?

A

Each one has multiple functions, often in the brain and in the peripheral nervous system which are separated by the blood brain barrier

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13
Q

What things about neurotransmitters are unique?

A

Each neurotransmitter has:

  • Its own anatomical distribution
  • Its own range of receptors it acts on
  • Its own range of functions in different regions (some separated by the blood brain barrier)
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14
Q

What is the anatomical distribution of dopamine?

A
  • Brain stem
  • Basal ganglia
  • Limbic system and frontal cortex
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15
Q

What physiological functions are affected by dopamine?

A
  • Voluntary movement
  • Emotions/reward
  • Vomiting
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16
Q

What pathways does dopamine act in?

A
  • Mesolimbic
    • Projects VTA to nucleus accumbens and other limbic structures
    • Role in reward and addiction
    • Overactivity leads to schizophrenia and hallucinations
  • Mesocortical
    • Projects to frontal cortex
    • Involved in executive function
    • Impairment relevant for cognitive symptoms (sx) in PD
  • Tubero-infundibular
    • Inhibits prolactin
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17
Q

What is the mesolimbic pathway?

A

Projects VTA to nucleus accumbens and other limbic structures

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18
Q

What does overactivity of the mesolimbic pathway lead to?

A

Schizophrenia and hallucinations

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19
Q

What is the mesocortical pathway?

A

Projects to frontal cortex

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20
Q

The mesolimbic pathway has a role in what?

A
  • Role in reward and addiction
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21
Q

The mesocortical pathway has a role in what?

A
  • Involved in executive function
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22
Q

What does the tubero-infudibular pathway do?

A
  • Inhibits prolactin
23
Q

What is PD caused by?

A

Degeneration of DA cells in the SN (nigrostriatal)

24
Q

How does PD impact dopamine?

A

Caused by degeneration of DA cells in the nigrostriatal so causes dopamine deficiency in the basal ganglia

25
Q

Describe the synthesis of dopamine?

26
Q

How can dopamine synthesis be modulated in vivo?

A

Pharmacologically block the conversion of DOPA to dopamine in the periphery, so DOPA crosses the blood brain barrier into the brain and is converted to dopamine there

27
Q

Are any dopamine receptors ionotropic?

A

No (so dopamine cannot evoke fast EPSPs or IPSPs)

28
Q

What class of receptors are dopamine receptors?

A

Metabotropic (ie g-protein coupled)

29
Q

How many different subtypes of metabotropic dopamine receptors are there?

A

5 subtypes named D1 - D5

30
Q

Dopamine can produce many different effects, and different effects in different brain regions. What does this depend on?

A

Which receptors are expressed

31
Q

What protein are dopamine receptors coupled to?

A

Adenylate cyclase

32
Q

What dopamine receptors activate adenylate cyclase?

33
Q

What dopamine receptors inhibite adenylate cyclase?

A

D2, D3 and D4

34
Q

Describe the metabolic breakdown of dopamine?

35
Q

What are key enzymes in the breakdown of dopamine?

A

Monoamine oxidase B (MAO-B)

Catechol-O-methyltransferase (COMT)

36
Q

What is dopamine ultimately broken down into?

A

Homovanillic acid

37
Q

What are symptoms of PD?

A
  • Stiffness
  • Slow movements
  • Change in posture
  • Tremor
38
Q

What are examples of dopaminergic drugs?

A
  • DA precursor
    • Levodopa
  • DA agonists
    • Ergots
      • Bromocriptine, pergolide, cabergoline
    • Non-ergots
      • Ropinirole, pramipexole, rotigotine
    • Apomorphine
39
Q

Why are dopaminergic drugs used in the treatment of PD?

A

Ease PD symptoms

40
Q

What are some enzyme inhibitors used for preserve dopamine levels?

A
  • Peripheral AAAD inhibitors
    • Such as carbidopa and benserazide
    • Decreases peripheral side effects of levodopa and allows greater proportion of oral dose to reach CNS
  • MAOB inhibitors
    • Such as selegiline, rasagiline and safinamide
  • COMT inhibitors
    • Such as entacapone and opicapone
    • Decreased metabolism of dopamine and increased effectiveness of levodopa
41
Q

Drug treatment of PD targets what?

A

Dopaminergic neurons

42
Q

What are some possible side effects of dopaminergic drugs?

A
  • Worsen or cause
    • Nausea
    • Vomiting
    • Psychosis
    • Impulsivity/abnormal behaviours
43
Q

Dopamine antagonists improve what?

A
  • Nausea
  • Vomiting
  • Psychosis
44
Q

Dopamine antagonists can cause what?

A
  • Worsen or cause
    • Parkinsonism
45
Q

How can antagonitsts that do not cross the blood brain barrier improve vomiting?

A

Area postrema (vomiting centre) is in the medullar and functionally outside the blood brain barrier

46
Q

What is the vomiting centre called?

A

Area postrema

47
Q

What drug is used to treat vomiting in PD patients?

A
  • Domperiodne
    • DA antagonist
    • Anti-emetic
    • Does not cross blood brain barrier
    • No antipsychotic properties
    • Relatively safe to use in PD
    • Has permitted the therapeutic use of apomorphine (which is a powerful emetic)
48
Q

What is dyskinesias?

A

Abnormal involuntary movements

49
Q

Which of DA agonists and DA antagonists cause dyskinesias?

50
Q

What can long term DA antagonist use lead to?

A
  • Antipsychotics/anti-dizziness
  • Often cause parkinsonism
    • Such as receptor blockade in basal ganglia
  • Sometimes cause dyskinesias
    • Tardive dyskinesias (orofaciolingual)
      • Upregulation or increased sensitivity of certain DA (dopamine) receptors
51
Q

GABA agonists are used to treat what?

A

Anti-epilepsy drug

Also have anti-anxiety properties

52
Q

Serotonin is used to treat what?

A
  • Selective serotonin reuptake inhibitors (SSRIs) are antidepressants
  • Triptans (selective 5HT agonists) used for the treatment of migraine
53
Q

Noradrenaline is used to treat what?

A
  • Reuptake blockers such as tricyclic drugs are antidepressants
  • MAO inhibitors are antidepressants

nervous system (48 decks)

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