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NEURO > Applied Neuro-Pharmacology > Flashcards

Applied Neuro-Pharmacology Flashcards

1
Q

Sequence of events in synaptic transmission?

A
  1. Packaging of neurotransmitter in presynaptic terminals
  2. Na AP in presynaptic terminal
  3. AP opens Ca gated channels
  4. Ca triggers package of neurotransmitter exocytosis
  5. Transmitter diffuses across cleft, binds receptors
  6. Transmitter inactivated by uptake or by extracellular breakdown
  7. Transmitter metabolized
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2
Q

What sort of manipulations to synaptic transmission could reduce synaptic transmission?

A
  1. Block AP (local anaesthetics)
  2. Block Ca channels
  3. Block transmitter release
  4. Block postsynaptic receptors (allows for selectivity)
  5. Increase transmitter breakdown / uptake
  6. Inhibit transmitter synthesis
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3
Q

What sort of manipulations to synaptic transmission could increase synaptic transmission?

A
  1. Use a transmitter agonist

2. Block transmitter break down / uptake

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4
Q

What class of transmitter is dopamine?

A

Monoamine

  • along with noradrenaline & serotonin
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5
Q

What can help separate transmitters in the brain from having adverse actions elsewhere in the body (eg. in the PNS)?

A

The blood brain barrier

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6
Q

Where is dopamine anatomically distributed in the brain?

A
  • Brain stem
  • Basal Ganglia
  • Limbic system and Frontal cortex
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7
Q

Which physiological functions are affected by dopamine?

A
  • Voluntary movement
  • Emotions / reward
  • vomiting
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8
Q

Where does the mesolimbic pathway run between? What brain functions is it involved in?
Consequences of overactivity?

A
  • Ventral Tegmental Area (VTA) of midbrain to Ventral Striatum of the basal ganglia
  • Involved in motivation and reward
  • Overactivity leads to positive schizophrenia sx and hallucinations in PD
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9
Q

Where does the mesocortical pathway run between? What brain functions is it involved in?
Consequences of impairment?

A
  • Connects VTA of midbrain to prefrontal cortex
  • Involved in executive function and cognition
  • Impairment causes reduced cognition in PD and effects in schizophrenia
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10
Q

What are the four main dopaminergic pathways of the brain?

A
  • Mesocortical
  • Mesolimbic
  • Nigrostriatal
  • Tubero-infundibular
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11
Q

What is the Tubero-infundibular pathway involved in?

A
  • Inhibition of prolactin

hormone for producing breastmilk

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12
Q

Where does the nigrostriatal pathway extend from?

What is its main function?

A
  • Connects the substantia nigra with the basal ganglia

- Critical in the production of movement as part of the basal ganglia motor loop

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13
Q

What causes the effects of Parkinson’s Disease (PD)?

A

Degeneration of dopaminergic cells in the substantia nigra (SN)

  • Therefore dopamine deficiency in basal ganglia
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14
Q

Precursors during dopamine synthesis?

A
  1. Glycine
  2. Alanine
  3. Phenylalanine
  4. Tyrosine
  5. DOPA (dihydroxyphenylalanine)
  6. Dopamine
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15
Q

What type of receptor does dopamine act on? How many subtypes of receptor are there for dopamine?

A
  • Metabotropic (G-protein coupled)

- 5 different subtypes of receptor (all either activate or inhibit adenylate cyclase)

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16
Q

What is the consequence of dopamine having multiple different receptors?

A
  • Dopamine can have many effects, and produce different effects in different brain regions depending on which receptors are expressed
17
Q

What are the key enzymes in dopamine breakdown?

A
  • Monoamine oxidase B (MAO-B)

- Catechol-O-methyltransferase (COMT)

18
Q

What effects does the loss of dopamine cause in PD?

A
  • Stiffness
  • Slow movements
  • Change in posture
  • Tremor
19
Q

What are some dopaminergic drugs?

A

Dopamine Precursor:
- Levodopa

Dopamine Agonists:

  • Ergots (bromocriptine, pergolide)
  • Non-Ergots (ropinirole, pramipexole)
  • Apomorphine

(improve some symptoms of PD)

20
Q

What enzyme converts DOPA to Dopamine? Where can it be blocked? Effects of blockage?

A
  • AAAD
  • Can be blocked in the PNS (carbidopa),
  • reduces peripheral side effects of PD and allows more DOPA to reach CNS
21
Q

What is the effect of MAOB and COMT inhibitors?

A

Reduce the metabolism of dopamine

  • Therefore increase effectiveness of levodopa
22
Q

What are the positive effects of dopaminergic drugs?

A

Improve:

- Some motor features of PD, eg: limb rigidity, bradykinesia and tremor

23
Q

What are the negative effects of dopaminergic drugs?

A
  • Nausea
  • Vomiting
  • Psychosis
  • Impulsivity / abnormal behaviours
24
Q

What symptoms of Parkinson’s are not helped by dopaminergic drugs?

A

Midline Features, eg:
- Dysarthria (unclear speech)

  • Balance
  • Cognition
25
Q

What is the effect of dopamine antagonists?

A

Opposite of dopaminergic drugs:
- Improve: vomiting, nausea and psychosis

  • Worsen: Parkinsonism
26
Q

Where is the vomiting centre of the brain? How can this help vomiting treatment?

A
  • The area postrema (vom centre) is in the medulla, but is functionally OUTSIDE the BBB
  • Allows possibility for Dopamine antagonist that doesn’t cross BBB to be used to treat vomiting
27
Q

What is the dopamine antagonist that doesn’t cross the BBB and so can be used to treat vomiting? Is it safe to use in PD patients?

A

Domperiodne

  • Relatively safe for PD patients, no antipsychotic properties though
28
Q

What is a drug that induces vomiting called? What is one that stops vomiting called?

A
  • Emetic

- Anti-emetic

29
Q

What is a dyskinesia?

How do dopaminergic drugs and dopamine antagonists relate to dyskinesia?

A
  • Dyskinesia: abnormal involuntary movements
  • Dopaminergic drugs may cause dyskinesia (too much movement)
  • DA antagonists may cause parkinsonism (not enough movement)
30
Q

What are dopamine agonists usually used to treat? What can their long term use cause?

A
  • Function as Antipsychotics / anti-dizziness drugs
  • Can cause Parkinsonism (receptor blockade in basal ganglia)
  • Can cause dyskinesia (complicated - due to increased sensitivity of certain dopamine receptors)

NEURO (52 decks)

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