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Clinical Neurology > Biochem-Ch. 48 > Flashcards

Biochem-Ch. 48 Flashcards

1
Q

What are the important peptide neurotransmitters?

A

Beta-endorphin

Met-enkaphalin

Leu-enkaphalin

Somatostatin

Substance P

Neurotensin

Vasoactive intestinal peptide

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2
Q

What is the important difference between the peptide NT and the small molecule NT?

A

-The peptide NT are heteropolymers of amino acids (peptides)

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3
Q

What are the small molecule NT of importance?

A

Acetylcholine

Dopamine

Norepinepherine

Epinepherine

Serotonin

Melatonin

Histamine

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4
Q

Which of the NT are derived from tyrosine?

A

DA, Epi, and NE

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5
Q

Which of the small molecule NT are derived from Tryptophan?

A
  • 5-HT (serotonin) and Melatonin
  • remember these are bicyclic compounds
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6
Q

Which of the small molecule NT is derived from Histadine?

A

-Histamine…DUR

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7
Q

What are the impiortant amino acid NT?

A

Glutamate (Glu)

Aspartate (Asp)

Glycine (Gly)

GABA (gamma-aminobutyric acid)

Serine (Ser)

Cysteine (Cys)

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8
Q

What are the important purigenic or nucleic acid NT?

A

Adenosine

ATP

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9
Q

What are the three catcholamines? What are they derived from?

A
  • Dopamine, NE and Epi
  • Tyrosine–> which can be made from phenylalanine, therefore the catecholamines can be derived from either
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10
Q

What enzyme is responsible for the conversion of phenylalanine to tyrosine in the liver?

A

-Phenalanine hydroxylase

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11
Q

What is the rate limiting enzyme in the sythesis of catacholamines? What does it catalyze?

A
  • Tyrosine hydroxylase
  • catalyzes the conversion of tyrosine to Dopa (L-DOPA)
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12
Q

What coenzyme is required for the conversion of L-Tyrosin to L-Dopa by tyrosine hydroxylase?

A

Tetrahydrobiopterin (BH4)

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13
Q

Where is tyrosine hydroxylase found?

A

-only in catecholamine cells

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14
Q

What enzyme and therefore pigment is lacking or defective in individuals with albinsism?

A
  • A defect in the copper dependant tyrosine hydroxylase of melanocytes (different than TH in the adrenal medulla)
  • no conversion of DOPA to melanin
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15
Q

What enxyme is responsible for the conversion of L-DOPA to Dopamine?

A

DOPA decarboxylase

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16
Q

Where does the DOPA decarboxylase reaction take place?

A

In the cytoplasm

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17
Q

What is the immediate precursor to NE?

A

Dopamine (DA)

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18
Q

What enzyme is responsible for the conversion of DA to NE?

A

Dopamine-ß-hydroxylase or DbH

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19
Q

What cofactors are essential for the conversion of DA to NE by dßh?

A
  • Vitamin C
  • O2
  • Cu
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20
Q

What enzyme is responsible for the conversion of NE to Epi?

A

phenylethanolamine N-methyl-transferase

(PMNT)

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21
Q

What coenzyme is required by PMNT for the conversion of NE to Epi?

A

SAM

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22
Q

What is required for the synthesis of SAM?

A

Folic Acid and vitamin B12

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23
Q

What is the general pathway requiring the use of B12 and Folic acid?

A
  • Folic Acid donates a methyl group to B12
  • B12 then donates that methyl group to homocysteine–>methionine which eventually forms SAM.
  • That methyl group is then donated to the substrate and SAM is recycled.

**note the difference in NE and Epi is the addition of a methyl group! Neat-o

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24
Q

What would the result of a deficiency vitamin C?

A

Lack of dßh function

–> leading to a lack of conversion of DA to NE

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25
Q

A defect in the SAM pathway (folic acid or B12 deficiency) would lead to a build up of what small molecule NT?

A

NE

-SAM converts NE–>Epi

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26
Q

After conversion from L-DOPA to DA in the cytosol, where are the NT moved?

A

-Into starage vesicles where the conversion from DA to NE will take place in NE containine neurons

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27
Q

What is the enzyme responsible for the transport of catcholamines into vesicles?

A

Vessicle monoamine transporter 2

(VMAT2)

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28
Q

What small NT conversions take place in the cytosol?

A

L-tyrosine–> L-DOPA –> Dopamine

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29
Q

What transformations, if needed, take place in storage visicles?

A

DA–> NE

and

NE–> Epi

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30
Q

How does proton pumping play into the transport of catecholamines into storage vesicles?

A

-A high proton concentraction (acidic) is establised inside of the vesicle by and H+/ATP pump

The efflux of H+ is then linked to the influx of catecholamines through this secondary active transport

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31
Q

How many transmembrane domains does VMAT2 have?

A

12

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32
Q

What is a chromogranin?

A

the soluble content of a storage vesicle

-includes NT and d

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33
Q

How is reuptake of NT after release mediated?

A

-Through Na dependant reuptake

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34
Q

What is the role of monoamine oxidase (MAO) in catecholamine degredation?

A

-oxidizes the carbon containing amino group to an aldehyde

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35
Q

How does Catechol-O-methyltransferase (COMT) help to inactivate catecholamines?

A

-transfers a methyl group from SAM to the extracellular catcholamine.

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36
Q

Since COMT employs the use of SAM, what coenzymes are indirectly required for its proper operation?

A

-vitamin B12 and Folate

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37
Q

What is tyramine? What does it have to do with MAO?

A

-Tyramine is the degradation product of Tyrosine

Tyramine is usually inactivated by MAO-A

38
Q

Are the metabolisms of NE and Epi similar?

A

Yes, almost identical

39
Q

What is homovanillylmandelic acid (HVA) a marker of?

A
  • Dopamine turnover
  • typically found in the CSF, Blood and urine
40
Q

What is VMA an indicator of?

A

NE and Epi turnover

41
Q

How is tyrosine hydroxylase inhibited?

A

-by free cytosolic catecholamines

(if catecholamines are high, TH does not want to make more)

42
Q

What factors contribute to the activation of TH during neuronal stimulation?

A

-Depolarization of the neuron activates PkA and PkC which phosphorylate TH and result in tight binding of it to BH4

43
Q

What is the long term effect of excess stimulation of TH and dopamine levels?

A

Prolonged stimulation results in the increase of TH and Dopamine in the nerve terminals.

44
Q

How is the synthesis of 5-HT similar to dopamine synthesis?

A
  • a similar enzyme (tryptophan hydrogenase) is used in the conversion of tryptophan to 5-HT
  • then the exact same enzyme DOPA decarboxylase is used in the decarboxylation of 5-HT to serotonin
45
Q

Is the coenzyme used by tryptophan hydroxylase similar to the one used by TH?

A

-Yep. Exactly the same one–> BH4

46
Q

In the conversion of Serotonin to melatonin, what enzyme is common?

A

-conversion of SAM to SAH in the methyl transfer of N-acrtylserotonin–> melatonin

47
Q

What enzymes assists in the breakdown and inhibtion of DA and serotonin?

A

-MAO

48
Q

Is visicle uptake and storage of 5-HT similar to that of DA? How does it differ?

A
  • Yes (secondary active Via H+ gradient)
  • Transport by both VMAT1 and VMAT2
  • binds to 5-HT binding protein (Iron heme) once in the vesicle
49
Q

How do MAO-Is treat depression?

A

-They block the breakdown of 5-HT, NE and DA in the wall of the mitochondria and increase their concentration

50
Q

What is an SSRI? What is it used to treat?

A
  • Selective serotonin reuptake inhibitor
  • Blocks the reuptake of 5-HT and used to treat depression
51
Q

What kind of drugs are 5-HT1 agonists?

A

Anti-anxiety drugs

52
Q

What drug is a 5-HT2 agonist? So then

A

-LSD

53
Q

What receptors do antipsychotics act on?

A

5-HT2 antagonists

54
Q

What are 5-HT3 antagonists used for?

A

The treatment of chemotheraphy nausea

55
Q

How is the degrdation of histamine different from most other NT?

A

Histamine is not recycled into the presynaptic terminal

56
Q

Where is histamine inactivated and degraded?

A

Astorcytes

57
Q

What cells use histamine in thebrain?

A

Mast cells

58
Q

What enzyme is resposible for the synthesis of Acetylcholine?

A

Choline Acetyltransferase

(ChAT)

59
Q

What is the location of ACh synthesis?

A

-Presynaptic terminal

(then it is transferred into vesicles)

60
Q

Where does the choline for acetylcholine norammyl come from?

A
  • Common part of the diet
  • Can also be synthesized as part of the synthesis of phospholipids
61
Q

How is vitamin B12 indirectly involved in the synthesis of choline?

A

-In the endogenous synthsis of choline, methyl groups are sequentially added by SAM.

–> SAM needs vitamin B12 to reconstitute its methyl group

62
Q

Is the mechansim for transport of ACh similar to other NT?

A

Yes.

  • 12 membrane H+ countertransporter
  • H+/ATP pump
63
Q

What enzyme is resposible for the inactivation of acetylcholine?

A

-Acetylcholinesterase

64
Q

How can glutamate be synthesized from glutamine?

A

With the use of glutaminase

65
Q

Where does the glutamine used to sythesize glutamate come from?

A

Glial cells

66
Q

What TCA cycle intermediate can be converted into glutamate? What are the two ways in which this can take place?

A
  • Alpha-ketogluterate
  • this can be accomplised by either adding free ammonia to glutamate or by transamination from other amino acids.
67
Q

How is GABA synthesized?

A

-by decarboxylation of glutamate

68
Q

What enzyme is responsible for the decarboxylation of glutamate to GABA?

A

Glutamic acid decarboxylase

69
Q

How are GABA and glutamate deactivated and transported?

A
  • Glial cells uptake GABA which is converted to glutamate
  • this and the rest of the glutamate is then converted to glutamine and transported to neurons where it is converted back to glutamate
70
Q

What is the main function of aspartate?

A

-Excitatory NT, cannot pass through the BBB

71
Q

What is the main function of glycine?

A

-Major inhibitory NT of the spinal cord

72
Q

What is the only Metabotropic triggered outward potassium channel? Is it inhibitory or excitory?

A

GABAB

-inhibitory

73
Q

From what AA is NO synthesized from?

A

Arginine

74
Q

What are the functions of NO?

A
75
Q

How much of the oxygen supply of the body does the brain use?

A

20%

76
Q

What is the brain’s main supply of energy? What can it use during persiods of fasting or development?

A
  • Glucose is the main fuel
  • Ketone bodies can be used if absolutely needed
77
Q

When the blood glucose falls below 45mg/dL what does the brain first try to use as fuel?

A

-internal substrates like glutamate and TCA cycle intermediates

78
Q

Why does neural activity begin to fall as teh blood glcose level drops below 45mg/dL?

A

The brain reduces sythesis of certain NT.

79
Q

What happens if blood glucose falls below 1mM or 18mg/dL?

A
  • ATP supplies are depleated
  • neruonal death insues as the EEG becomes isoelectric
80
Q

What NT are most dependant on glucose levels?

A

Glycine

Aspartate

Glutamate

81
Q

What is the cause of cognitive dysfunction in hypoxic patients?

A

Impaired neurotransmitter synthesis

82
Q

Does mild hypoxia cause an increase or a decrease in the blood supply to the brain?

A

Increase to maintain O2 delivery

83
Q

What is the effect of glutamate synthesis on the energy system of the brain?

A

Glutamate synthesis removes Alpha-ketogluterate from the TCA cycle causing a reduction in oxaloacetate.

-Slows down the TCA cycle

84
Q

How does the BBB impact lipid transfer into the brain?

A

BBB restricts the movement of non-essential fatty acids across the barrier. (Palmitate)

85
Q

Which lipds can enter the brain?

A

-Essential fatty acids like:

–lioleic acid

–linolenic

86
Q

Which lipids are synthesized within the brain?

A

Cholesterol

Glycerol

Sphingolipids

glycophingolipids

Cerebrosides

-Very long chain fatty acids used in myelin formation

87
Q

How and where are the brains very long chain fatty acids catabolized?

A

-Within peroxisomes by alpha-oxidation

88
Q

What is myelin?

A

A multilayered lipid and protein structure that is formed from the plasma membrane of glial cells

PNS: Schwann cell–> sinlge axon

CNS: oligodendrocyte–> multiple axons

89
Q

What are the two most important structural myelin proteins?

A
  • Myelin basic protein (MBP)
  • proteolipid protein
90
Q

What is important about antibodies directed against MBP?

A

-Helps in the understanding of MS

91
Q

Is MBP positively charged or negatively charged? What face of the myelin membrane does it lie upon?

A
  • Positively charged
  • cytoplasmic face

Clinical Neurology (8 decks)

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