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Biochemistry > Semester 3: Midterm 1 > Flashcards

Semester 3: Midterm 1 Flashcards

1
Q

What is an ionophore? Function?

A

A lipid-soluble molecule usually synthesized by microorganisms to transport ions across the lipid bilayer of the cell membrane

Have antibiotic properties

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2
Q

Conformations of Na/K-ATPase?

A

E1 : high affinity for Na and ATP (0,2mikroM)

E2 : low affinity for ATP (150mikroM)

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3
Q

Subunits/structure of Na/K-ATPases? Function and location of different subunits

A

Dimer, one alpha and one beta subunit
Might have a gamma subunit as well

a: 10TM, breaks ATP, has phosphorylation site, binds both Na, K

a1; most cells, epithelial cells
a2; striated muscle, brain, heart
a3; neurons, heart
a4; testis

b: anchor to mem., regulation

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4
Q

Inhibitor of Na/K-ATPase?

A

Ouabain

(Has a secondary effect on Ca2+ - sodium, calcium exchanger - reversed: Na out, Ca in -> pos. inotropic effect (inc. force of contr.))

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5
Q

Tissue specific hormonal regulation of Na/K-ATPase?

A

1)Dopamine:
- prod. in prox. tubules, inhibits here and in cortical coll. tubules
- dec. Na reabsorption
2)E/NE:
- E: Skeletal muscle- stim. K uptake (dec. hyperkalemia after exercise)
- NE: Kidney- DA antagonist -> Na reabsorption
Brain- reestablishment if ion gradient after nerve impulse
3)Insulin:
- Skeletal muscle- translocation of enzyme to PM
4)Aldosterone:
- Kidney- adaptation to dec./inc. Na/K intake respectively

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6
Q

Function of the FXYD subunit

A
  • Regulates the catalytic function of the alpha subunit of Na/K-ATPases.
  • FXYD1 (heart) - dec. Na affinity of alpha subunit when dephosphorylated
  • FXYD2 (kidney) - inc. affinity for ATP
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7
Q

Function of H/K-ATPase

A

K-absorption and H-excretion

Located in stomach parietal cells

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8
Q

Plasma membrane calcium ATPases

A

PMCA1: General
PMCA2: neuronal
PMCA3: striated muscle, brain
PMCA4: General

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9
Q

P-type-ATPases

A

1) Na/K-ATPase
2) H/K-ATPase
3) SERCA-ATPase
4) Plasma membrane calcium ATPase
5) Na/H exchanger

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10
Q

SERCA ATPases

A

SERCA1: striated muscle

2: smooth muscle, striated muscle, heart muscle (ALL muscle types)
3: platelets endothelial cells + other non-muscle cells

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11
Q

Na/H exchanger isoforms, location

A

5 isoforms and 12TM regions
NHE1: General - BL mem.
NHE3: Epithelial cells - Apical mem.
NHE5: Brain and testis

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12
Q

Types of the vesicular monoamine transporters, function, inhibitor

A

(12TM - broad selectivity: E/NE, dopamine, serotonin)
VMAT1: Brain, neuroendocrine cells
VMAT2: neurons, adrenal chromaffin cells
VAchT: cholinergic synapses

Function: generation of a pH around 6 inside the cell -> generates a chemical pot. -> cotransport of protons out of vesicle, NT into vesicle

Inhibitor: H ionophores

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13
Q

Where can we find cholinergic transmission by Acetylcholine?

A

1) NM-junction
2) Autonomic preganglionic fibers (nicotinic receptors)
3) Parasympathetic post ganglioside fibers to heart, glands, smooth muscle (muscarinic receptors)
4) CNS

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14
Q

How is choline taken up in the axon terminal? Inhibitor?

A

Cotransport with Na, inhibitor hemicholiniums

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15
Q

How is ach synthesized?

A

Acetyl-Coa + Choline –> CoA + Ach

Catalyzed by choline acetyltransferase

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16
Q

How is Ach taken up into vesicles?

A

By VAchT

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17
Q

Describe the process of vesicular exocytosis of Ach

A

1) NT uptake into vesicles, cluster formation (reserve pool)
2) Docking: to active zone
3) Priming: Formation of SNARE complex + association of synaptotagmin (UNSTABLE INTERMEDIER)
4: Fusion: Calcium influx –> synaptotagmin C2 domain partially inserted into membrane –> NT released

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18
Q

SNARE proteins in synaptic exocytosis

A

In vesicles: Synaptobrevin + VAMP (vesicle associated membrane protein)
In PM: Syntaxin 1A/B + SNAP-25

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19
Q

Inhibitor of cholinergic neurotransmission?

A

Botulinium toxins

- Has a heavy chain and a light chain

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20
Q

What is the inhibitor of muscarinic receptors?

A

Atropine

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21
Q

List the muscarinic receptors and their function

A

QIQQ
M1: Gq coupled -> Ca increase (so reg. of NT release)
M2: Gi coupled -> cAMP dec. (found in heart)
Binding of Ach -> act. K channels -> BRADYCARDIA
M3: Gq -> smooth muscle contraction, secretion stimulation (in GI tract)

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22
Q

What are the inhibitor(s) of nicotinic receptors?

A

Curare

Alpha-bungarotoxin (venom from a snake)

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23
Q

What subunits are found in nicotinic receptors?

A

5 subunits

  • muscle type (embryonic): alpha1, beta1, gamma, delta
  • muscle type (adult): alpha1, beta1, delta, epsilon
  • neuronal type: alpha3,beta2 OR alpha5??
  • The receptor is a ligand gated cation channel
  • 2 Ach binds to aplha subunit to open channel
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24
Q

Where can we find nicotinic receptors?

A

Striated muscle (leads to contraction)

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25
Q

What causes malignant hyperthermia?

A
  • Complication of inhaling anesthetics
  • Mutation in RYR1 receptor —> Large Ca inc. intracellularly
    Gives hypermetabolism -> fever + muscle rigidity
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26
Q

What enzyme hydrolyzes Ach in the synaptic cleft?

A

Acetylcholinesterase

Gives choline + acetate

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27
Q

What causes myasthenia gravis? Treatment?

A
  • Circulating antibodies in the synaptic cleft inhibiting the postsynaptic nicotinic Ach receptors
  • Treatment: reversible acetylcholinesterase inhibitors
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28
Q

What is the main NE producing center in the brain and what does it innervate?

A 
Locus ceruleus (in rhomboid fossa)
Innervates: cerebral cortex, thalamus, hypothalamus, olfactory bulb, cerebellar cortex, midbrain and spinal cord
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29
Q

What is the common precursor of catecholamines?

A

Tyrosine

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30
Q

What is the rate-limiting step in the synthesis of NE?

A

Tyrosine hydroxylase (1st step)

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31
Q

How is NE synthesis regulated?

A

1) Neg. fb inhibition by NE
2) Activation by Ca
3) Phosphorylation by PKA, PKC and Calcium/Calmodulin dependent kinase (inc. affinity for pterin cofactor)
4) When symp. aff. is inc. -> inc. in tyrosine hydroxylase -> NO neg. fb inhib (+calcium entry to axon terminals)
5) Long-term activity -> amount of enzyme inc.
6) Steroid hormones inc. act. of N-methyltransferase -> inc. synthesis of E

32
Q

What can L-dopa be used to treat?

A

Parkinson’s disease

33
Q

How is catecholamines taken up by vesicles?

A

By VMTA2

34
Q

What is the inhibitor of VMTA2?

A

Reserpine (irreversible inhib.)

35
Q

What is MAO and where can it be found?

A

Monoamine oxidase, will deaminate catecholamines in axon terminal. Found in mitochondria (outer mem.)

  • MAO A: Prefer NE and serotonin
  • MAO B: Synthetic substrates and dopamine
36
Q

What is the inhibitor of MAO A?

A

Clorgilin

37
Q

What is the inhibitor of MAO B?

A

Deprenyl (med. in Parkinson’s)

Selegilene – diff. name

38
Q

What does COMT stand for and what is it’s role?

A

Catechol-O-Methyl-Transferase degrades catecholamines by transfer of methyl to 3-hydroxy group

39
Q

What is the main metabolite of NE metabolism in the brain?

A

MHPG (appears in CSF and urine)

40
Q

What are inhibitors of uptake of catecholamines at presyn. mem.?

A

Cocain, tricyclic antidepressants

41
Q

What adrenergic receptors do we have?

A

QISSS - alpha 1+2, beta 1-3 (g-protein coupled)

42
Q

What is the effect of beta1 adrenergic receptors?

A

Cardiac: Increased inotropic and chronotropic effect
GI tract: Smooth muscle relaxation
(Stim. of lipolysis)

43
Q

What is the effect of beta2 adrenergic receptors?

A

Uterus: Smooth muscle relaxation
Skeletal muscle: Mobilisation of glycogen, vasodilation
Bronchi: Dilation
(Inc. glyconeogenesis, glycogenolysis)

44
Q

What is the effect of beta3 adrenergic receptors?

A

Stimulation of lipolysis

45
Q

What is the effect of alpha1 adrenergic receptors?

A

Smooth muscle contraction (vasoconstriction)

Increased glycogenolysis

46
Q

What is the effect of alpha2 adrenergic receptors?

A

Smooth muscle contraction (vasoconstriction)
Inhibition of NT release
(Inhib. lipolysis + platelet aggregation)

47
Q

Dopamine works on D1 receptors and gives …… effect

A

Excitatory (inc. movements/thoughts/emotions)

48
Q

Dopamine works on D2 receptors and gives …… effect

A

Inhibitory (inc. movements/thoughts/emotions)

49
Q

What structures are included in the reward system? (dopaminergic)

A

Ventral tegmental area, frontal cortex, nucleus accumbens, striatum, substantia nigra, hippocampus

50
Q

What is the function of amantadine?

A

It’s a weak antagonist of the NMDA type glutamate receptor, inc. dopamine release, blocks dopamine reuptake

51
Q

List the different dopamine receptors and their function

A
  • D1 and D5: act. adenylate cyclase -> cAMP -> PK
    also acts on TFs that binds on CRE (long term response) + IEG -> gene transcription + prot. translation
  • D2: Inhibition od adenlylate cyclase
  • D3 and D4: Not much is known
52
Q

What drugs can be used in the therapy of parkinson’s disease?

A

1) L-dopa (Levodopa)
2) Deprenyl
3) Dopamine receptor agonist

53
Q

Why should carbidopa be given with levodopa?

A

Because levodopa is converted to dopamine in the PNS and excessive eripheral dopamine signaling gives side effects. Carbidopa bypasses these side effects so levodopa can enter brain!

Carbidopa prevents levodopa from being converted to dopamine in the periphery (dopamine cannot enter the brain once converted from levodopa)

54
Q

What is characteristic for schizophrenia?

A
  • Increased dopaminergic activity -> Inc. dopamine levels, inc. levels of homovanillic acid in urine, inc. nr. of D2 receptors
  • Decreased glutaminergic activity
55
Q

Where is serotonin produced and what is it’s other name?

A 
Produced in: 
-Brain -> pineal gland
-Retina
-Platelets
-GI tract
Other name: 5-hydroxytryptamine (5-HT)
56
Q

What are the effects of serotonin?

A
  • Depressed appetite, elevated mood, make you agressive

- Elevates levels of ACTH, GH, Prolactin

57
Q

When do we have the most melatonin/serotonin and why?

A
  • We have most melatonin at night because there is more N-acetyl transferase
  • Most serotonin during the day because it’s not converted to melatonin as much
58
Q

How is serotonin taken up into vesicles?

A

Done by serotonin-H exchanger (using proton gradient made by proton transporter)

59
Q

How is serotonin taken up by PM?

A

By a transporter called SERT using the gradients of Na, K and Cl (Na+Cl in, K out)

60
Q

The process of vesicle uptake of serotonin and PM uptake is inhibited by…?

A
  • Fenfluramine and amphetamine derivatives (enhances NT release)
  • Ecstasy+cocaine inhibiting both –> more serotonin in synaptic cleft –> better mood, depressed appetite
61
Q

Serotonin receptors

A

5-HT1 : Associated with mood
5-HT2 : Involved in hallucinations -> LSD is an agonist
5-HT3 : In sensory neurons in GI tract -> connected with the feeling og nausea
5-HT1B,D,F : Associated with migraines

62
Q

List 3 antidepressive drugs

A

1) Inhibitors of MAO
2) SERT inhibitors
3) 5-HT1A receptor agonists

63
Q

How do we study ion channels?

A

With the patch clamp technique

64
Q

Definition of open probability

A

The time a channel stays open/total observation time

65
Q

How does voltage and ligands affect gating in ion channels?

A

By altering the rate constants

66
Q

What is throughput rates?

A

The amount of ions transported through the channel at a given time

67
Q

Can the ion channel be saturated?

A

Yes

68
Q

Structure of K-channel

A
  • 4 separate protein units
  • Each unit: 6TM helices (each separated by P-loop)
  • Shape of an inverted teepee
  • Gate is IC
  • Selectivity filter: (EC side) K can only be present in 1st and 3rd position, or 2nd and 4th
69
Q

How is a voltage gated K channel activated?

A

Arg + Lys residues on 4th helix function as voltage sensors -> depol. -> changes conformation of these

70
Q

How is inactivation of voltage gated K channels eliminated?

A

By enzymatic cleavage (trypsin), or artificial depletion (deltaN) of N terminus

71
Q

List 3 voltage gated K channels and the diseases associated with them (as well as location and role)

A

Kv1.1:
- Location: CNS and PNS, dendrites, axon terminals
- Role: Repol. after AP
- Mutations: Ataxia, myokymia
KCNQ1, HERG:
- Location: Ventricular myocytes
- Role: Repol. after AP
- Mutations: long QT syndrome -> ventricular fibrillation, sudden death
KNQ2/3:
- Location: Neurons (hippocampus, symp. ganglia)
- Role: Dereased excitability
- Mutations: Benign familial neonatal epilepsy

72
Q

Structure of ATP-sensitive K channels

A
  • Octamers
  • 4 pore forming K channels (Kir6.2)
  • 4 sulfonylurea receptor (SUR) subunits
  • SUR: 3 TMDs, 2 IC NBDs
73
Q

The ATP-sensitive K channels shows inward rectification, what blocks ion current outwards?

A
  • Intracellular Mg2+

- Polyamines

74
Q

Where can we fin Kir6.2 and SUR1, what is its role and possible mutations?

A
  • Location: Pancreatic beta cells
  • Role: Insulin secretion
  • Mutations: Persistent hyperinsulinaemic hypoglycemia (PHHI) and type2 diabetes
75
Q

Structure and location of the CFTR channel

A 
Structure:
- 2 TMDs
- 2 IC NBDs
- 1 regulatory domain
Found in pancreas, intestines, lungs, sweat glands
76
Q

What binds to the intracellular/extra cellular side of Na/K-ATPase?

A

Intra: Na, ATP
Extra: K, Ouabain

Biochemistry (9 decks)

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