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BIOL 125 > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

What is a catechol group?

A

Phenol ring with -OH groups in 3 and 4 positions.

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2
Q

What are catecholamines synthesised from in the body?

A

Tyrosine.

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3
Q

What 4 major transmitters are catecholamines?

A

Adrenaline, Noradrenaline, Dopamine, Serotonin.

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4
Q

Why is Tyr transported into the brain from the blood?

A

Because the brain lacks phenylalanine hydroxylase (enzyme that converts Phe to Tyr).

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5
Q

Which transmitter is associated with motor function and lost in Parkinson’s disease?

A

Dopamine.

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6
Q

Catabolism of catecholamines is performed by which 2 enzymes?

A 
Monoamine oxidase (MAO),
Catechol 0-methyltransferase (COMT).
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7
Q

How is Dopamine synthesised from Tyrosine?

A

Tyrosine reacted with enzyme Tyrosine β-hydroxylase, forming L-Dopa.
Dopa reacted with enzyme Dopa decarboxylase forming Dopamine.

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8
Q

How is Noradrenaline synthesised from Dopamine?

A

Dopamine reacted with enzyme β-hydroxylase forming Noradrenaline.

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9
Q

How is Adrenaline formed from Noradrenaline?

A

Noradrenaline reacted with enzyme Phenylethanolamine N-methyl transferase (PNMT), forming Adrenaline.

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10
Q

Who was Parkinson’s first described by and when?

A

James Parkinson. 1817.

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11
Q

Mean age of onset of Parkinson’s?

A

~60 years.

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12
Q

How many over 65s does Parkinson’s affect?

A

1-2%.

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13
Q

Three main symptoms of Parkinson’s?

A

Muscle rigidity, tremor, bradykinesia.

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14
Q

Parkinson’s is a multifactorial disease. Name 3.

A

Age.
Environmental factors.
Genetics.

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15
Q

What happens neurologically in Parkinson’s?

A

Degeneration of pigmented cells of the ‘substantia nigra pars compacta’ in basal ganglia.

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16
Q

What does Parkinson’s result in neurologically?

A

> 50% depletion of Dopamine.

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17
Q

What catecholamine is administered to treat Parkinson’s disease, and what is it converted into?

A

L-DOPA.

Transported to brain and converted to dopamine.

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18
Q

Why is a Dopa decarboxylase inhibitor simultaneously administered alongside the L-DOPA when treating Parkinson’s?

A

Because this inhibitor can’t penetrate into the brain, and so prevents the rest of the body metabolising the L-DOPA into Dopamine, which can’t cross the blood-brain barrier.

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19
Q

What inhibitors can also be administered to reduce Dopamine degradation?

A

Inhibitors of MAO and COMT.

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20
Q

What is serotonin (5-HT) synthesised from, and via which enzymes?

A

Synthesised from tryptophan, using tryptophan hydroxylase and 5-hydroxytryptophan (5-HTP) decarboxylase.

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21
Q

How many different types of 5-HT receptors are there?

A

14.

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22
Q

What class of drugs can act as 5-HT agonists, mimicking serotonin at 5-HT2A receptors?

A

Hallucinogenic drugs, e.g. LSD.

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23
Q

How is serotonin action terminated?

A

Mainly by re-uptake from synapse via 5-HT re-uptake transporter on presynaptic neurone.

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24
Q

By what enzyme can 5-HT be catabolised (therefore inactivated)?

A

MAO.

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25
Q

What is the intermediate product between L-Tryptophan and Serotonin?

A

5-Hydroxy-L-Tryptophan (5-HTP)

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26
Q

In what system are amino acids found at the highest concentration in the body? What concentration is this?

A

CNS.

30mM.

27
Q

What type of amino acids are found in the CNS? And what are they made from?

A

Non-essential amino acids.

Made in situ from glycolytic and citric acid intermediates.

28
Q

What are the 4 amino acids found in the brain?

A

Glu, Asp, Gly, GABA.

29
Q

Which amino acids in the brain are excitatory?

A

Dicarboxylic amino acids (glutamate, aspartate).

30
Q

Which amino acids in the brain are inhibitory?

A

Monocarboxylic amino acids (Glycine and GABA)

31
Q

Which 2 amino acids are MAJOR transmitters in the brain?

A

Glycine and GABA.

32
Q

How many known examples of small peptide transmitters are there?

A

Around 100.

33
Q

Where are small peptide transmitters the most common?

A

Hypothalamus.

34
Q

As what are peptide transmitters first synthesised, where are they transported, and how are they activated?

A

Synthesised as large precursor proteins,
Transported to synaptic release site,
Activated by proteolytic cleavage.

35
Q

Are peptide transmitters fast or slow?Do peptide transmitters exhibit fast or slow postsynaptic effects?

A

Slow.

36
Q

What molecules terminate peptide transmitters?

A

Extracellular proteases.

37
Q

Peptide transmitters are often co-released, but with what?

A

Other classical transmitters.

38
Q

Opioids are one type of peptide transmitter. Three types of endorphins?

A

Endorphins, Enkephalins, Dynorphins.

39
Q

3 other examples of peptide transmitters (except opioids)?

A

Substance P, neurotensin, vasoactive intestinal peptide (VIP).

40
Q

3 other transmitters, not part of the aforementioned groups?

A

Purines (ATP, GTP, etc.)
Histidine
Gases - Nitric Oxide (NO).

41
Q

Is NO stored?

A

No - synthesised in synaptic vesicles. Made as required.

42
Q

What enzyme synthesises NO, and from what?

A

NOS, from arginine.

43
Q

How does NO work?

A

Diffuses from nerve terminals into adjacent cells, forming covalent linkages to a multiplicity of targets.

44
Q

How is NO presumed to inactivate?

A

Diffuse away.

45
Q

2 types of transmitter receptor?

A 
Ionotropic receptor (transmitter acts DIRECTLY on ligand gated ion channel to open channel).
Metabotropic receptor (transmitter acts INDIRECTLY on G protein-coupled receptor).
46
Q

Are ionotropic receptors always stimulatory?

A

Yes.

47
Q

How quick are ionotropic and metabotropic receptors?

A

Ionotropic very fast - few milliseconds.

Metabotropic very slow - up to hours.

48
Q

Sequence of events for transmitter receptors? (7)

A
  • Agonist binds to receptor.
  • GTP exchange for GDP on G protein α-subunit.
  • G protein dissociates from receptor, then ligand.
  • 3 subunits (α, β, γ) of G protein also dissociate.
  • α-subunit activates ion channel.
  • α-subunit inactivated by hydrolysis of GTP (to GDP) (by GTPase).
  • α-subunit combines with β and γ subunits, attaching to receptor, which can then bind new agonist.
49
Q

What else can G proteins act on, besides ion channels.

A

Enzyme targets - stimulating (Gs), or inhibiting (Gi).

50
Q

What are the most common enzymes targeted by G proteins? And what are their corresponding second messengers?

A

Adenylate cyclase - cyclic AMP (cAMP).
Guanylate cyclase - cyclic GMP (cGMP).
Phospholipase C - inositol triphosphate and diacylglycerol.

51
Q

Composition of ligand-gated receptors?

A

4 or 5 different subunits arranged around central pore in the membrane.

52
Q

Four examples of ligand-gated receptors?

A

nicotinic acetylcholine, GABAA, glycine, 5-HT3 receptors.

53
Q

How many subunits is the nicotinic receptor composed of?And how many different subunits are there in total generally? - what does this mean for the diversity of the receptors?

A

5.

17 generally. Means there are different combinations in skeletal muscle, autonomic ganglia, brain.

54
Q

How do nicotinic ligand-gated receptors work?

A

α-subunit binds to acetylcholine, resulting in a conformational change opening the central ion channel.

55
Q

What are G-protein coupled receptors composed of?

A

7 membrane spanning regions (α-helices).

56
Q

Another name for G-protein coupled receptors?

A

7TM (seven transmembrane receptor).

57
Q

5 examples of 7TMs?

A 
Muscarinic acetylcholine, 
α-adrenergic and β-adrenergic receptors, 
all 5HT receptors apart from 5HT3,
rhodopsin, 
olfactory receptors.
58
Q

What do tricyclic antidepressants target?

A

(depression) block noradrenaline and serotonin uptake.

59
Q

What do SSRIs target?

A

(depression, OCD) block serotonin uptake.

60
Q

What does Valium and other benzodiazepines target?

A

(anxiety) activate GABA receptors.

61
Q

What do MAO inhibitors target?

A

(depression, Parkinson’s) block breakdown of biogenic amines.

62
Q

What does L-DOPA target?

A

(Parkinson’s) a dopamine precursor.

63
Q

What do Acetylcholinesterase inhibitors target?

A

(Alzheimer’s) block breakdown of acetylcholine.

BIOL 125 (11 decks)

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