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Flashcards in MT1: Mats Short Answers Deck (29)
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1
Q
  1. Name the enzymes of this reaction (included picture of Choline + AcetylCoa → Ach + CoA)
  2. Where is this enzyme located
A
  1. Choline acetyltransferase

2. Presynaptic terminals of cholinergic neurons

2
Q

Indicate one therapeutical means by which the synthesis of NE can be decreased

A

AMPT
alpha-methyl-p-tyrosine

(used in adrenal medulla cancer)

3
Q
  1. Which nT is released from the motor neurons stimulating contraction
  2. Through which receptor is this effect mediated
  3. What is the second messenger essential for the above effect
A
  1. Acetylcholine
  2. n-Ach-R
  3. Increase in [Ca2+]ic
4
Q

List the consecutive intermediates in NE synthesis

A

L-tyrosine → DOPA → dopamine → NE

5
Q

How does dopamine influence the kidney:

  1. The activity of the Na+/K+ ATPase
  2. The rate of Na+ absorption
A

Dopamine is a natiuretic hormone:

  1. Dopamine inhibits the basolateral Na+/K+ ATPase
  2. Dopamine (→PKA) decreases activity of Na+/H+ exchanger (NHX) in the luminal membrane, thus decreasing Na+ entry into the cell
6
Q

Name the main metabolite formed in the brain in NE metabolism, which can be detected in urine

A

MHPG

3-methoxy-4-hydroxy-phenylglycol

7
Q

Name a hormone that stimulates the activity of the Na+/K+ ATPase

A

Aldosterone

8
Q
  1. What is the name of the enzyme that hydrolyses Ach in the synaptic cleft
  2. What kind of molecule exerts an irreversible inhibition on this molecule
  3. What is the underlying clinical effect of this inhibition
A
  1. Acetylcholinesterase
  2. DFP (Diisoproylfluorophosphate) or other organic phosphate-molecules (mustard gas).
    The phosphate molecule covalently binds to the ser-residue of the active center
  3. Inhibition of AchE will lead to accumulation of Ach in the synaptic cleft causing prolonged stimulation (paralysis) and eventually death (respiratory)
9
Q
  1. What is the primary target of strophantine/oubain in the human body
  2. What is the sequence of events that leads to positive inotropic effect by strophantine
A
  1. Inhibits cardiac myocyte Na+/K+ ATPase
  2. Accumulation of Na+ → NCX works in opposite direction → accumulation of Ca2+ → increased contractility

(too much leads to ↑↑Ca2+ which leads to tetanic contractions → death)

10
Q

Ion channels are protein pores that span the ….?

A

Plasma membrane

11
Q

The open probability of an ion channels range from/to?

A

From 0-100 % (Po = Time in open state / total observed time)

12
Q

At high ionic concentrations the ion channel throughput rates becomes …. ?

A

Saturated

13
Q

The protein segment responsible for the K+ channel selectivity is called the …?

A

Pore loop

14
Q

The selectivity filter of the K+ channel is located close to the …?

A

Extracellular side

15
Q

The central cavity communicates with which solution through the gate?

A

Incracellular solution

16
Q

During N-type inactivation the N-terminal peptide segment of the voltage-gated K+ channel plugs its pore from which side?

A

N-terminal is located on the intracellular side

17
Q

ATP-sensitive K+ channels are involved in the regulation of which hormone

A

Insuline secretion from Betacells (but also glucagon)

18
Q

Type II diabeetus mellitus can be treated by sulphonylureas.

What effect do they have on the ATP-sensitive K+ channels?

A

Sulfonylureas (tolbutamide) inhibits the ATP-sensitive K+ channels by binding to the SUR1-subunit. This leads to depolarization → Ca2+ → Insulin release

19
Q

What effect does phosphorylation by PKA have on the CFTR

A

Ser-residues in the intracellular regulatory domain are phosphorylated and activated. This is the physiological activator of the channel

20
Q

Under physiological conditions ATP-sensitive K+ channels are:

  1. Activated by?
  2. Inhibited by?
A
  1. Activated by intracellular ADP (ic regulatory domains) and by diazoxide (TM region of SUR subunits)
  2. Inhibited by high intracellular ATP (e.g. ↑glucose) → depolarization → Ca2+ → Insulin

(remember sulfonylureas also inhibits!)

21
Q

Which techniques reveals openings and closures of individual ion channel pores?

A

Patch clamp technique

22
Q

ATP-sensitive K+ channels are heterooctamers formed by four IRK-subunits (inward rectifying K-channel)
Which type are the last four receptor subunits?

A

Sulfonylurea receptor (SUR1, 2, 3 and 4)

23
Q

What does the phosphorylated CFTR channel need for gating?

A

ATP

24
Q

Why does ecstasy cause a drastic release in serotonin?

question is weird, but basically what does ecstasy do
Fenfluramide does the same

A

Ecstasy and Fenfluramide inhibits both the vesicle- and plasmamembrane transporter, leading to accumulation of serotonin in the cleft AND increased release from presynapstic

25
Q

Name an enzyme that makes NO, and what is it made from

A

Nitric Oxide Synthase (NOS), made from arg

26
Q

What is the action of phenylethanolamine N-methyl-transferase?

A

NE + SAM → E + SAH

27
Q

How does the AMPA receptor act on the NMDA receptor

A

AMPA alows Na+ influx → slight depol → Mg2+ is removed from NMDA → NMDA allows Na+ and Ca2+ influx → long-term and high depol

28
Q

What are the inhibitors of NE?

A

MAO and COMT

29
Q

What is the molecule that regulates the Ca2+ic directly?

A

IP3