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Biochemistry II > Ch 46 Metabolism of the Nervous System > Flashcards

Ch 46 Metabolism of the Nervous System Flashcards

1
Q

What is the role of dendrites on a neuron? Axons?

A

The role of dendrites on a neuron is to receive information from the axons of other neurons.

The role of axons is to transmit information to other neurons.

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2
Q

How many axons does a nerve have? Dendrites?

A

Neurons contain ONE axon, but these branch extensively and distribute information to multiple targets (divergence)

Neurons contain many dendrites, each receiving signals from multiple axons.

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3
Q

What must a dendrite have to respond to a specific neurotransmitter?

A

specific receptor

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4
Q

How does a neuron send a signal to multiple cells?

A

extensive axonal branching to multiple targets

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5
Q

What stage of differentiation are neurons in?

A

terminally differentiated

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6
Q

can neurons divide?

A

no, terminally differentiated

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7
Q

What happens when a neuron is damaged?

A

Neurons that are injured or damaged have a limited capacity to repair themselves and frequently undergo apoptosis.

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8
Q

What is the role of astrocytes in the CNS?

A

provide physical and nutritional support for neurons
Phagocytosing debris left behind by cells,

Providing lactate (from glucose metabolism) as a carbon source for the neurons, and

Controlling the brain extracellular ionic environment.

Regulate the content of ECF by taking up, processing and metabolizing nutrients and waste products

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9
Q

What role do astrocytes play in development of the CNS?

A

guide neuronal migration to their final adult position and form a matrix that keeps neurons in place

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10
Q

Where are oligodendrocytes located and what is their major role? List 3 additional roles.

A

oligodendrocytes are found in the CNS where they provide myelin sheath that surrounds the axon, which insulates many neurons in CNS.
(along with astrocytes) Form a supporting matrix for neurons

Limited capacity for mitosis, so if damaged it will not replicate

Note: It can result in abnormalities in signal conduction along that axon

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11
Q

Where on the neuron is myelin? What cells produce myelin in the CNS? PNS?

A

The myelin is found around axons in both the CNS and PNS. The difference is myelin is produced by Oligodendrocytes in the CNS and Schwann cells in the PNS.

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12
Q

Can oligodendrocytes divide?

A

no

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13
Q

Name 2 cell types that provide a supporting matrix for neurons in the CNS

A

oligodendrocytes and astrocytes

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14
Q

do damaged oligodendrocytes replicate?

A

no; They have limited capacity for mitosis and if damaged do not replicate.

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15
Q

If oligodendrocytes are damaged, what may happen to neurons?

A

demyelination of the axons which can result in abnormalities in signal conduction along the axon

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16
Q

How many axons can oligodendrocytes myelinate? Schwann cells?

A

Oligodendrocytes can myelinate multiple axons while Schwann cells myelinate only one axon.

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17
Q

If a peripheral neuron’s axon is damaged, can it be regenerated?

A

yes

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18
Q

Which brain cells serve an immunological function?

A

Microglial cells serve as immunologically responsive cells. They destroy invading microorganisms and phagocytose cellular debris.

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19
Q

What type of cells do the microglial cells resemble in circulation?

A

macrophages

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20
Q

Which cells in the brain have cilia? What are the cilia for?

A

Ependymal cells are ciliated cells that line the ventricles of the CNS and the spinal cord. The cilia are for efficient circulation of the CSF throughout the CNS.
Note: in some areas of the brain, they elaborate and secrete CSF into the ventricular system

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21
Q

Where are ciliated cells located?

A

line the cavities (ventricles) of the CNS and spinal cord

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22
Q

Some of the ciliated cells can produce ____

A

CSF

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23
Q

What type of stem cells has recently been found within the ependymal cell layer?

A

neural stem cells

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24
Q

Name the cell types of the CNS and PNS that can perform phagocytosis

A

CNS: astrocytes, ependymal, microglia
PNS: Schwann cells and microglial cells

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25
Q

How does the interstitial fluid composition resemble that of blood?

A

Similar due to the rapid passage of molecules from the blood through the endothelial wall into the interstitial fluid.

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26
Q

What two processes that normally occur in endothelial cells are missing from those in the brain?

A

transcapillary movement and transendothelial transport (fenestratrions and transpinocytosis)

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27
Q

What type of enzyme systems are present in endothelial cells of the brain?

A

drug metabolizing enzyme system for the metabolism of toxic chemicals and neurotransmitters

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28
Q

the drug metabolizing enzyme system of the brain is similar to that of which other organ?

A

liver

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29
Q

What do P-glycoproteins do? What do they need for this?

A

Pump hydrophobic molecules (or xenobiotics) out of the brain and into the blood. They are transmembranous, ATP-dependent efflux pumps.

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30
Q

Name four molecules or types that can passively diffuse across the BBB

A

water, oxygen, CO2, lipophilic substances

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31
Q

What is needed for choline to cross the BBB?

A

Phosphatidylcholine (from blood via a low-affinity transport system and from the synaptic cleft via high-affinity transport mechanism)

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32
Q

What type of fatty acids can and cannot cross the BBB?

A

Nonessential fatty acids cannot cross the BBB, essential fatty acids are transported across the BBB

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33
Q

Name the glucose transporters on the endothelial cells, neurons and glial cells.

A

Endothelial cells – both membranes via facilitated diffusion via GLUT1 transporter

Neurons – GLUT3 transporters

Glial cells – GLUT1 transporters

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34
Q

Which two cell types are referred to as “glial” cells?

A

oligodendrocytes and astrocytes

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35
Q

What can you infer is the approximate Km of GLUT1 (in mg/dL)?

A

60 mg/dL

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36
Q

In a person with normal blood [glucose] but 0.4X normal CSF [glucose] (hypoglycorrhachia), what transporter might be deficient?

A

GLUT1

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37
Q

Name 5 monocarboxylic acids that can be transported across the BBB into the brain.

A

L-lactate

Acetate

Pyruvate

Acetoacetate (ketone body)

Beta-hydroxybutyrate (ketone body)

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38
Q

What type of amino acids enter the brain through a single transporter. Which amino acid does it prefer? What do these AAs have in common?

A

Large neutral amino acids (LNAAs) F, L, Y, I, V, W, M, H enter via single amino acid transporter – L system amino acid transporter

It prefers Leucine, hence the “L” system name.

These are essential amino acids and must be imported for protein synthesis or as precursors for neutrotransmitters.

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39
Q

Can essential fatty acids cross the BBB?

A

yes

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40
Q

Why is entry of small neutral amino acids into the brain restricted?

A

The entry of small neutral amino acids is restricted because their influx could dramatically change the content of neurotransmitters.
Note: some examples of small neutral amino acids include A, G, P, and GABA

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41
Q

How do vitamins enter the brain?

A

Vitamins have specific transporters through the blood-brain barrier, just as they do in most tissues

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42
Q

List 3 proteins known to cross the BBB by receptor-mediated endocytosis.

A
  1. insulin
  2. transferrin
  3. insulin-like growth factors
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43
Q

What are the two categories of neurotransmitters?

A
  1. small nitrogen-containing molecules

2. neuropeptides

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44
Q

What does “adrenergic tract” mean?

A

Neuronal tract that synthesizes and releases the neurotransmitter epinephrine and norepinephrine.

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45
Q

What organ has opioid receptors?

A

Brain. Opioid receptors located within CNS

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46
Q

What type of neurotransmitter binds opioid receptors?

A

endorphins

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47
Q

what is the effect of endorphins?

A

block pain signals

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48
Q

What are two neuropeptide hormones that are synthesized in the brain but released into circulation?

A

GH and TSH

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49
Q

Where in the cell are neurotransmitters synthesized?

A

In the cytoplasm of the presynaptic terminal. Most of these neurotransmitters are synthesized from amino acids, intermediates of glycolysis and the TCA cycle and O2

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50
Q

How do the synthetic enzymes get to the site of neurotransmitter synthesis?

A

Transported by fast axonal transport from the cell body, where they are synthesized, to the presynaptic terminal

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51
Q

What is required to transport neurotransmitters into vesicles?

A

An ATP dependent pump linked to a proton gradient transports the NTs into the vesicles. So ATP is required.

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52
Q

What results from depolarization of the presynaptic membrane?

A

An influx of Ca2+ ions through voltage gated calcium channels

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53
Q

What is the signal that triggers vesicle fusion with the presynaptic membrane?

A

Influx of Ca2+

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54
Q

How is the neurotransmitter signal transmitted to the post-synaptic neuron?

A

Diffusion across synaptic cleft. Transmission of synapse is completed by binding of the neurotransmitter to a receptor on the postsynaptic membrane

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55
Q

List 4 ways that a neurotransmitter signal can be terminated.

A
  1. Reuptake into the presynaptic terminal
  2. Uptake into glial cells
  3. Diffusion away from the synapse
  4. Enzymatic inactivation
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56
Q

List 4 places that enzymatic inactivation of a neurotransmitter can occur.

A

Postsynaptic terminal

Presynaptic terminal

Adjacent astrocyte microglial cells

Endothelial cells in the brain capillaries

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57
Q

Name 2 reactions of catecholamine synthesis that require biopterin (BH4).

A

Phenylalanine → tyrosine → L-Dopa; steps 1 (phenylalanine hydroxylase) & 2 (tyrosine hydroxylase)

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58
Q

What is the rate-limiting step of catecholamine synthesis?

A

Hydroxylation of tyrosine via tyrosine hydroxylase, which requires BH4

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59
Q

Melanocytes produce a distinct tyrosine hydroxylase. What is it dependent on?

A

copper (Cu2+)

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60
Q

What condition results from a deficiency of melanocyte tyrosine hydroxylase?

A

albinism

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61
Q

What does DOPA stand for?

A

Dihydroxyphenylalanine

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62
Q

Dopa decarboxylase requires what co-factor and results in _____ of Dopa to _____.

A

Like many decarboxylation reactions, Dopa decarboxylase requires pyridoxal phosphate. Results in decarboxylation of Dopa to dopamine.

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63
Q

Some neurons produce an additional enzyme, ____ that converts Dopamine to ____.

A

Some neurons produce beta-hydroxylase found only within storage vesicles. They convert dopamine to norepinephrine.

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64
Q

Where is this enzyme located in the cell?

A

DBH is an enzyme found in storage vesicles of these cells

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65
Q

What 3 things does this enzyme require for its activity?

A

Cu2+ bound cofactor required for the electron transfer

Vitamin C – electron donor

O2

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66
Q

What is the electron donor in the dopamine beta-hydroxylase reaction ?

A

Vitamin C

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67
Q

What is the electron donor in the reaction above?

A

Transfer of methyl group converts NE to epinephrine. The cofactor required is SAM.

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68
Q

Epinephrine synthesis is dependent on which vitamins?

A

Vitamin B12 & folate (B9) in order to produce SAM

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69
Q

Why does transport of dopamine into vesicles require ATP?

A

Due to the high concentration of dopamine in storage vesicles, transporting more dopamine into vesicles would require ATP.

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70
Q

What is transported in opposition to dopamine? What is the name of this transporter?

A

A Proton is transported in opposition to dopamine via Vesicle Monoamine Transporter 2 (VMAT2)

Note: VMAT2 is homologous to p-glycoprotein. Also, H+ exchanged for positively charged catecholamines. p. 961

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71
Q

What does VMAT2 transporter have homology to?

A

Family of bacterial drug-resistance transporters, including P-glycoprotein

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72
Q

What is the ATP used for in the catecholamine storage transport system?

A

ATP is used for the proton pump, V-ATPase

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73
Q

What do call the type of transport used in the transport of catecholamines into storage vesicles?

A

secondary active transport

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74
Q

What are chromogranin? What are they complexed with?

A

Chromogranin are acidic proteins that are complexed with ATP and catecholamines in NT storage vesicles

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75
Q

How is catecholamine signaling terminated?

A

Catecholamine signaling is terminated through reuptake into the presynaptic terminal and diffusion away from the synapse. Degradative enzymes are present in the presynaptic terminal and in adjacent cells, including glial cells and endothelial cells.

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76
Q

What are the 2 major catecholamine degradative enzymes?

A

COMT and MAO

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77
Q

Which enzyme is located on the outer mitochondrial membrane? What does it remove from catecholamines?

A

MAO. It removes an ammonium ion by oxidizing the carbon (containing the amino group) to an aldehyde.

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78
Q

What additional compound (besides VMA) is produced when any catecholamine is oxidized?

A

NH4+, ammonium

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79
Q

Which isoform preferentially degrades serotonin and norepinephrine?

A

MOA-A

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80
Q

What enzyme uses SAM as a cofactor? What is the activity of this enzyme?

A

COMT; it transfers a methyl group from SAM to a catecholamine or its degradation product

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81
Q

Parkinson disease patients have _______________ in their CSF, indicating _______ degradation.

A

PD patients have decreased levels of cebrospinal homovanillymandelic acid (HVA) indicating dopamine degradation

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82
Q

What is a breakdown product of catecholamines that is excreted in the urine?

A

metanephrine

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83
Q

What supplies feedback inhibition of tyrosine hydroxylase?

A

Free cytosolic catecholamines compete at the binding site of the enzyme for cofactor, pterin.

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84
Q

How do free cytosolic decrease tyrosine hydroxylase activity?

A

These free cytosolic catecholamines decrease the activity of tyrosine hydroxylase by competing at the binding site of the enzyme for pterin cofactor (BH4)

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85
Q

What activates tyrosine hydroxylase?

A

The depolarization of the nerve terminal activates tyrosine hydroxylase

86
Q

List 3 kinases that are activated by depolarization

A

PKC

PKA (cAMP dependent protein kinase)

CAM kinases (Ca2+-calmodulin dependent [CAM] kinases)

87
Q

How do specific kinases activate tyrosine hydroxylase?

A

These phosphorylate tyrosine hydroxylase making it tighter to BH4 making it less sensitive to end-product inhibition

88
Q

Longer term activation of catecholamines is accomplished by increased production of ____ &______.

A

Tyrosine hydroxylase and DBH

89
Q

Increased transcription of specific genes is thought to result from increased _________ binding to ________.

A

This is due to phosphorylation of CREB by PKA which leads to CREB binding to CRE in the promoter region of the gene.

90
Q

What is the first enzyme and cofactor in serotonin synthesis?

A

The first enzyme and cofactor in serotonin synthesis are tryptophan hydroxylase which requires BH4 to hydroxylate the ring structure of tryptophan

91
Q

What happens in the second reaction of serotonin synthesis? What cofactor is involved?

A

The second reaction of serotonin synthesis is a decarboxylation. The cofactor involved is PLP. It involves the same enzyme in dopa decarboxylation (dopa decarboxylase)

92
Q

The enzyme used in the second step of serotonin synthesis also uses __________ as a substrate

A

Dopa

93
Q

Two reactions are required to convert serotonin into melatonin. What are they?

A

Serotonin -> N-acetyl serotonin (N-acetylation – Acetyl-CoA)

N-acetyl serotonin -> Melatonin (O Methylation – SAM)

94
Q

Is melatonin production dependent on B12 and folate?

A

Yes, because it is dependent on SAM.

95
Q

The first reaction in serotonin breakdown is catalyzed by ____ and also produces _____.

A

MAO-A, ammonia (NH3)

96
Q

The second reaction in serotonin breakdown converts 5-hydroxyindole acetaldehyde to _______ and produces ______.

A

5-hydroxyindole acetic acid; NADH

97
Q

What does heparin induced thrombocytopenia have to do with serotonin?

A

The heparin induces accumulation of anti-heparin antibodies which indirectly cause release of serotonin. Therefore, depending on the concentration of heparin, serotonin levels may indicate HIT. For instance, when using low concentration of heparin, HIT is present if >20% is released. Also, when using high concentrations of heparin, if <20% is released it would also indicate presence of HIT.

98
Q

What happens when a person taking MAO inhibitor consumes red wine and cheese?

A

Those taking MAOI and consume red wine and cheese (which contain tyramine) would have increased levels of tyramine which induces the release of NE (from storage vesicles) and leads to life threatening hypertensive episodes.

Note: tyramine is a degradation product of tyrosine

99
Q

What compound accumulates in the “cheese effect”?

A

tyramine

100
Q

too much tyramine causes increased release of ___________

A

norepinephrine

101
Q

which symptom(s) of the cheese effect is possibly life-threatening?

A

hypertension

102
Q

What type of inhibitor is given for Parkinson disease but does not act as an antidepressant?

A

Deprenyl

Note: Clorygline is an antidepressant and suffers from the “cheese” effect.

103
Q

Inhibiting which enzyme is effective for anxiety and depression?

A

MAO-A

104
Q

An alternative to this enzyme inhibitor to treat anxiety & depression is a class of drugs called what?

A

SSRIs

105
Q

The first of these SSRI drugs, _____brand, _______generic, can cause mild weight loss.

A

The first of these drugs, __Prozac__ brand, __Fluoxetine__ generic, can cause mild weight loss.

106
Q

Two other SSRI drugs in this class are _____ and ______.

A

Two other drugs in this class are __Zoloft (Sertraline)__ and __Lexapro (Escitalopram).__

107
Q

Combining therapeutic doses of _____drugs with _____ over the counter medication could cause mild symptoms of serotonin syndrome.

A

Combining therapeutic doses of __SSRI__ drugs with __Dextromethorphan__ over the counter medication could cause mild symptoms of serotonin syndrome?

108
Q

What are the mild symptoms of serotonin syndrome?

A

Anxiety, agitation, restlessness, insomnia, tachycardia/tachypnea, hypotension/hypertension, dyspnea, flushing, diarrhea, incoordination, mydriasis, akathisia, ataxia

109
Q

Combining ____ with a tricyclic antidepressant or an ____ could result in more severe forms of serotonin syndrome.

A

Combining __SSRI__ with a tricyclic antidepressant or an __MAOI__ could result in more severe forms of serotonin syndrome.

110
Q

Histamine is produced from _____ in a _____ ______ reaction that requires ______ ______ cofactor.

A

Histamine is produced from __Histidine__ in a __single__ __enzymatic__ reaction that requires __pyridoxal__ __phosphate__ cofactor.

111
Q

What is the enzyme that produces histamine? What cofactor is required?

A

Histidine decarboxylase

PLP

112
Q

What 2 cell types in the brain can produce histamine?

A

Mast cells and certain neuronal fibers

113
Q

What is the first reaction for degradation of histamine in the brain? In what cells?

A

Methylation

Astrocytes

114
Q

The second reaction oxidizes methylhistamine & is catalyzed by _____, producing what by-product?

A

The second reaction oxidizes methylhistamine & is catalyzed by __MAO-B__, producing what by-product? NH4+

115
Q

A second oxidation results in ______ ____ ___ and ____.

A

A second oxidation results in __methylimidazole__ __acetic__ __acid__ and __NADH__.

116
Q

In peripheral tissues, histamine is oxidized by _____ ______.

A

In peripheral tissues, histamine is oxidized by __diamine__ __oxidase__.

117
Q

A second oxidation in peripheral tissues results in ____ ____ ___ and ____.

A

A second oxidation in peripheral tissues results in __imidazole__ __acetic__ __acid__ and __NADH__.

118
Q

Histamine in peripheral tissues is produced by ____ ______.

A

Histamine in peripheral tissues is produced by __histidine__ __decarboxylase__.

119
Q

Is histamine excitatory or inhibitory in the brain?

A

Excitatory

120
Q

What effect does histamine have in the lungs?

A

Airways constrict (in attempt to reduce intake of allergic material) so resulting bronchospasm, can lead to trouble breathing

121
Q

What is the enzyme that synthesizes acetylcholine?

A

Choline acetyltransferase (ChAT)

122
Q

What are the precursors of acetylcholine

A

Acetyl CoA and Choline

123
Q

How does choline enter the brain?

A

Choline is taken up by the presynaptic terminal from the blood

124
Q

Does the transporter from blood have a high or low Km?

A

Low affinity so high Km

125
Q

What in the brain can serve as a storage site for choline?

A

Membrane lipids from hydrolysis of phosphatidylcholine and possibly sphingomyelin

126
Q

Can humans synthesize choline? If yes, how?

A

Yes, as part of the pathway for the synthesis of phospholipids.

127
Q

Can choline be synthesized in the brain?

A

Yes in the liver and brain phosphatidylcholine is hydrolyzed to release choline or phosphocholine. Conversion of phosphatidylethanolamine to phosphatidylcholine occurs there.

128
Q

What vitamins are required for choline synthesis?

A

Folate and B-12 are required

129
Q

What is the source of acetyl groups for acetylcholine synthesis?

A

Acetyl-CoA

130
Q

Where in the cell is pyruvate converted to Acetyl CoA?

A

Pyruvate dehydrogenase is found only in mitochondria

131
Q

Acetylcholine is synthesized in the cytoplasm. How does Acetyl CoA get there?

A

Acetyl group transported to cytoplasm where it is cleaved in cytosol to form acetyl-CoA and OAA

132
Q

What enzyme inactivates acetylcholine? Where?

A

Acetylcholinesterase Neuromuscular junction

133
Q

What symptoms result from inhibition of this enzyme?

A

Paralysis

134
Q

What happens to the choline in the synapse?

A

Choline is taken up from the synaptic cleft via a high-affinity transport mechanism.

135
Q

Does the synaptic transporter have a high or low Km?

A

Low Km (high affinity)

136
Q

Does the placental choline transporter have a high or low Km?

A

Low Km (high affinity)

137
Q

In neonates, does the blood brain barrier choline transporter have a high or low Km?

A

Low Km (high affinity)

138
Q

What compound serves as the major dietary source of choline for neonates?

A

Phosphatidylcholine in Maternal milk

139
Q

Is glutamate excitatory or inhibitory in the brain?

A

Excitatory

140
Q

Is glutamate transported across the BBB?

A

No, not readily transported across the BBB.

Glutamate is synthesized de novo within nerve terminals because it’s plasma concentration is low

141
Q

What is the major source of glutamate precursors in the brain?

A

A-ketoglutarate

142
Q

Where does the glutamate precursor, A-ketoglutarate, come from?

A

TCA cycle or transamination of AAs

143
Q

Which 2 enzymes can convert this precursor to glutamate?

A

Glutamate dehydrogenase and PLP (transamination of AA to a-keto)

144
Q

Which one requires pyridoxal phosphate?

A

Transamination

145
Q

Another precursor for glutamate is _____, which comes from ____ cells.

A

Another precursor for glutamate is __glutamine__, which comes from __glial__ cells.

146
Q

Is GABA excitatory or inhibitory?

A

Inhibitory

147
Q

What is GABA synthesized from?

A

Glutamate

148
Q

GABA synthesis is a _____ reaction that requires____ as a cofactor.

A

GABA synthesis is a __decarboxylation__ reaction that requires __PLP (needs B12)__ as a cofactor.

149
Q

Most of GABA released at the synapse is taken up by ___ cells.

A

Most of GABA released at the synapse is taken up by __glial__ cells.

150
Q

These glial cells convert GABA to ____ via the ____ ____.

A

These glial cells convert GABA to __glutamate__ via the __GABA shunt__.

151
Q

Glutamate is converted to _____ in glial cells and released.

A

Glutamate is converted to __glutamine__ in glial cells and released.

152
Q

What cells take up the glutamine and convert it to glutamate?

A

Neurons

153
Q

Can glial cells synthesize GABA? Why or why not?

A

No, because they lack GAD.

154
Q

Epilepsy and other convulsant disorders can be treated by drugs that inhibit _____ __ ____ ___ ___ _____.

A

Epilepsy and other convulsant disorders can be treated by drugs that inhibit __reuptake__ of __GABA__ from the __synapse__.

155
Q

Can Aspartate cross the BBB?

A

No

156
Q

How is aspartate synthesized in the brain?

A

From the TCA cycle intermediate, OAA, via transamination reactions (which gets replaced via anaplerotic rxns)

157
Q

Is Aspartate excitatory or inhibitory?

A

Excitatory

158
Q

What is the major inhibitory neurotransmitter of the spinal cord?

A

Glycine

159
Q

What is Glycine synthesized from?

A

De novo (within the nerve terminal) from serine by serine hydroxymethyltransferase enzyme, which requires folic acid

160
Q

How is the signal produced by glycine probably terminated?

A

The uptake by a high-affinity transporter

161
Q

NO is synthesized from ____by the enzyme____

_____.

A

NO is synthesized from _arginine_______ by the enzyme___NO__ __synthase__.

162
Q

What type of cells produce large amounts of NO to kill microbes and tumor cells?

A

Macrophages

163
Q

What is the mechanism that NO uses to transduce a signal in endothelial cells?

A

NO readily crosses endothelial cell membranes —> activates guanylyl cyclase, which results in increased cGMP —> activation of protein kinases responsible for subsequent dilation of vessels

164
Q

What is activated to cause smooth muscle relaxation in blood vessels?

A

NO activates soluble guanylate cyclase for cGMP→ Protein Kinase activation → Vasodilation

165
Q

NO acts as a ________ to induce smooth muscle relaxation in the corpus _____.

A

NO acts as a __neurotransmitter__ to induce smooth muscle relaxation in the corpus __cavernosum to fill with blood (NO stimulates penile erection)__

166
Q

Where is the NO synthesized: pre or post-synaptic neuron?

A

Post-synaptic Neuron

167
Q

How is the NO signal terminated?

A

Phosphodiesterase breaks down cGMP

168
Q

What unique properties does NO possess compared to other neurotransmitters?

A

NO can cross the cell membrane because it is a gas

169
Q

Retrograde transmission involves release of neurotransmitters from the _____ _____ neuron.

A

Retrograde transmission involves release of neurotransmitters from the __presynaptic__ __terminal__ neuron.

170
Q

What property of NO allows it to stimulate neighboring cells?

A

Gaseous Substance

171
Q

How much of the body’s oxygen is used by the brain?

A

~20%

172
Q

What organelle is important for this?

A

Mitochondria (glc converted to pyruvate in glycolysis and then pyruvate oxidized in TCA cycle cycle)

173
Q

What is the major carbon source for the brain?

A

Glucose

174
Q

In addition to producing more ATP, what is provided by aerobic metabolism?

A

CO2

175
Q

What protective symptoms are initiated for protection against hypoglycemia?

A

Sweating, palpitations, anxiety, and hunger. Decreased Neurotransmitter synthesis

176
Q

Hypoglycemia symptoms initiate in the sensory nuclei of the _______.

A

Hypoglycemia symptoms initiate in the sensory nuclei of the Hypothalamus.

177
Q

How does the brain attempt to compensate for hypoglycemia?

A

The brain uses internal substrates such as glutamate and TCA cycle intermediates as fuel

178
Q

When blood [glucose] of 2-2.5 mM, symptoms are thought to arise from decreased _____ __ ________.

A

When blood [glucose] of 2-2.5 mM, symptoms are thought to arise from decreased __synthesis__ of __neurotransmitters __. (in particular regions of the brain rather than a global energy deficit)

179
Q

Decreased glucose availability is like to affect 3 neurotransmitters in particular. What are they?

A

Glycine, glutamate, GABA, aspartate

180
Q

Which pathways supply the precursors to the 3 neurotransmitters above?

A

Conversion of pyruvate to A-CoA in mito which generates a-ketoglutarate (for glutamate and GABA) and OAA (for aspartate), glycolysis - oxidation of glc to 3-PG (precursor for glycine)

181
Q

Which cells are most susceptible to death in hypoglycemia below 1mM glucose?

A

Neurons

182
Q

What neurotransmitter defect results from failure of energy-dependent reuptake pumps?

A

Glutamate excitotoxicity (build up of glutamate in cleft = overstim of postsynaptic glutamate receptors = prolonged activation = influx of lethal amounts of calcium ion = activation of cytotoxic intracellular pathways in postsyn neuron)

183
Q

Overstimulation of the _____ receptor leads to prolonged opening of the ___ ___ channel, leading to intracellular pathways of cytotoxicity in the _____ neuron.

A

Overstimulation of the __glutamate__ receptor leads to prolonged opening of the __Ca__ __Ion__ channel, leading to intracellular pathways of cytotoxicity in the __postsynaptic__ neuron.

184
Q

In mild hypoxia, what increases to maintain oxygen delivery to the brain?

A

Cerebral Blood Flow

185
Q

Even “moderate” hypoxia of paO2 25 mm Hg, severe cognitive dysfunction occurs. Why?

A

Impaired neurotransmitter synthesis

186
Q

In moderate hypoxia, what metabolic change occurs to maintain [ATP]?

A

Anaerobic glycolysis

187
Q

What changes occur with the metabolic switch above?

A

Increased lactate production and decreased pH (usually leads to coma)

188
Q

Why would pyruvate dehydrogenase activity be inhibited in the hypoxic brain?

A

Diminishes acetylcholine synthesis

189
Q

What neurotransmitter is especially dependent on this enzyme?

A

ACh

190
Q

When oxygen is unavailable to accept electrons, the concentration of ___increases.

A

When oxygen is unavailable to accept electrons, the concentration of __NADH__ increases.

191
Q

When the compound above increases, what pathway is inhibited?

A

TCA

192
Q

Name 2 major neurotransmitters that depend on TCA intermediates for their synthesis.

A

Glutamate and GABA

193
Q

Name the 2 major anaplerotic reactions that supply the TCA cycle.

A

Pyruvate carboxylase reaction and the Degradative pathway of branched chain amino acids, valine and isoleucine, which contribute succinyl coA to the TCA cycle (methylmalonyl CoA mutase)

194
Q

Which cells synthesize myelin in the CNS? PNS?

A

CNS - Oligodendrocytes.

PNS - Schwann cells

195
Q

What is the major type of component of myelin?

A

Lipids and proteins

196
Q

What type of fatty acid is especially enriched in myelin?

A

Cerebroside

197
Q

What are the 2 most prevalent proteins of myelin?

A

Proteolipid protein and myelin basic proteins (MBPs)

198
Q

Which myelin protein is easily extracted from membrane?

A

Myelin Basic Proteins (MBPs)

199
Q

Which protein is thought to stabilize the layered structure of myelin?

A

Proteolipid Protein

200
Q

Phosphatidylinositol is at higher concentration in the membrane of _____ termini

A

Phosphatidylinositol is at higher concentration in the membrane of __Postsynaptic__ termini

201
Q

List 4 membrane components that are constantly synthesized by the brain

A

Cholesterol, FA, glycosphingolipids, and phospholipids

202
Q

Which cell type surrounds only 1 axon?

A

Schwann Cell

203
Q

Which cell type surrounds multiple axons?

A

Oligodendrocytes

204
Q

What type of lipid is most highly enriched in myelin compared to other cell membranes?

A

Cerebrosides

205
Q

That choline is important for brain development is demonstrable by the high affinity transporters present in the placenta and at the neonatal BBB. Look at table 46.2 to determine why choline is so important.

A

More choline present in the gray matter so in the actual neurons, so choline deficiency inhibits development. In a developing brain even more choline is needed for the proper development of gray matter to occur.

206
Q

There is more cerebroside than phosphatidylcholine in myelin? What advantage does this confer?

A

Yes, specifically galactosylcerebroside

They pack more tightly together than phosphatidylcholine

207
Q

Refsum disease is due to a defect in ______ _____.

A

Refsum disease is due to a defect in __peroxisome__ __biogenesis__.

208
Q

Why would such a defect negatively affect the brain?

A

Severely affect brain cells because of the inability to metabolize both branched-chain and very-long-chain fatty acids.

209
Q

Which of the 2 demyelinating diseases discussed is autoimmune?

A

Multiple sclerosis (MS) and Charcot-Marie- Tooth polyneuropathy syndrome

210
Q

Which disease is a CNS defect?

A

Multiple sclerosis (MS)

211
Q

Which disease is a PNS defect?

A

Charcot-Marie-Tooth polyneuropathy syndrome

212
Q

What is the congenital defect in the PNS demyelinating disease?

A

Inherited mutations in P0 (major PNS myelin protein) - Autosomal dominant

Biochemistry II (2 decks)

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