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Biochemistry III > Cholinergic Neurotransmission > Flashcards

Cholinergic Neurotransmission Flashcards

1
Q

Where are cholinergic neurons located?

A
  • neuromuscular junction
  • autonomic preganglionic fibers
  • parasympathetic postganglionic fibers
    • heart, glands, smooth muscle
  • central nervous system
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2
Q

How is acetylcholine synthesized and where?

A

Acetyl CoA + Choline ⇔ CoA + Acetylcholine

catalyzed by choline acetyltransferase

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3
Q

Where is “low affinity” choline uptake and what is the KM ?

A

all tissues

KM > 10 μM

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4
Q

Where is “high affinity” choline uptake and what is the KM ?

A

only in cholinergic neurons

Na+ dependent

KM 1-5 μM

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5
Q

What is an inhibitor of “high affinity” choline uptake?

A

hemicholinium

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6
Q

Draw a schematic representation of how acetylcholine is taken into the vesicle.

A
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7
Q

What is the release of acetylcholine triggered by?

A

Ca2+

acion potential → depolarization of the axon terminal → Ca2+ entry via voltage-gated Ca2+ channels → exocytosis

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8
Q

Explain the process of exocytosis of the synaptic vesicles

A
  1. Uptake of neurotransmitter into vesicle
  2. Formation of cluster of vesicles- reserve pool
  3. Docking of vesicles in the active zone
  4. Priming- vesicles become competent for Ca2+ induced fusion
  5. Ca2+ signal- fusion (fusion pore- in the lipid bilayer
  6. Vesicle recycling
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9
Q

What are the different types of “recycling”

A
  • local recycling “kiss and stay”
  • fast recycling (reserve pool) no endosomal processing “kiss and run”
  • classical endocytosis
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10
Q

Are SNARE proteins and synaptotagmin involved in docking (stupid card)

A

NO

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11
Q

Explain the step of Priming in detail

A
  • formation of SNARE complex and association of synaptotagmin to the complex
  • vesicles and the plasma membrane are in close proximity

*unstable intermedier*

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12
Q

What does the Ca2+ signal induce?

A

the movement of synaptotagmin C2 domain into the phospholipid membrane

causes mechanical instability → fusion

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13
Q

Where are SNARE proteins located?

A

synaptic vesicles

plasma membrane

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14
Q

What are the SNARE proteins in the synaptic vesicles?

A

VAMP

(vesicle associated membrane protein)

Synaptobrevin

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15
Q

What are the SNARE proteins in the plasma membrane?

A

syntaxin 1A/B

SNAP-25

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16
Q

What provides the energy for the fusion of the vesicles and the plasma membrane?

A

SNARE motifs spontaneously form long

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17
Q

How many aminoacids do SNARE proteins contain?

A

70 aminoacid homolog sequence (SNARE MOTIF)

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18
Q

Describe the fusion-core complex.

A

paralell helices are formedwith the SNARE sequences that span into the cytosol (4 sequences from 3 proteins)

They are formed spontaneously in vitro between SNARE motifs

VAMP2- Syntaxin 1- SNAP 25

19
Q

Fusion of the v- SNARE and the t-SNARE schematic

A
20
Q

What do botulinum toxins do?

A

INHIBITORS of the cholinergic neurotransmission

in the cytosol LC (catalytic domain) it inhibits exocytosis

21
Q

Explain the components of botulinum toxins.

A

anaerob bacteria from clostridium botulinum

7 neuro-toxin

heavy chain (HC, 100kD) + light chain (LC, 50 kD)

22
Q

How are botulinum toxins taken up into the cholinergic terminals?

A

acceptor-mediated endocytosis

23
Q

What are botulinum toxins dependent on?

A

Zn2+ dependent endoproteases

absolute specificity for certain sites in the SNARE proteins

24
Q

What affects the stability of SNARE complexes?

A

can be increased or decreased by botulinum toxins

25
Q

Where are muscarinic receptors located?

A

organs innervated by postganglionic parasympathetic neurons

works via central nervous system

26
Q

What is the molecular mechanism of a muscarinic receptor?

A

PLC activation [Ca]

INHIBITION of adenylate cyclase

activation of K+ channels

27
Q

Where are nicotinic receptors located?

A

neuromuscular junction

28
Q

What is the molecular mechanism of nicotinic receptors?

A

Na+, K+ channels

29
Q

What effect do nictonic receptors have on striated muscle and the CNS?

A

ionotropic

30
Q

What is a muscarinic receptor antagonist?

A

atropine

31
Q

What is a nicotinic receptor antagonist?

A

curare

32
Q

What are the effects of nicotinic receptors on striated muscle?

A
  • Na+ and K+ permeability
  • membrane depolarization
    • Ca2+ release from SR
33
Q

What is a competitive inhibitor of nicotinic receptors in skeletal muscle?

A

D tubocuranine

34
Q

What is the effect of α-bungarotoxin?

A

Obtained from the venom of a snake

blocks muscular nicotinic receptors

35
Q

Events following the stimulation of nicotinic receptors in skeletal muscle

A
36
Q

What is malignant hyperthermia and what are the effects of it?

A

mutation of the ryanodin receptor

  • altered kinetics of Ca2+ channels
  • persistent long increase in [Ca2+]i

* can result in either*

a. ) hypermetabolism (fever)
b. ) persistent activation of the contractile system

(muscle rigidity)

37
Q

What is the function of acetylcholinesterase (serin protease)

A

hydrolysis of acetylcholine

(located within the synapse)

38
Q

What is acetylcholine esterase specific for?

A

acetylcholine

39
Q

What is the function of pseudocholinesterase?

A

hydrolysisof other esters

•short lasting muscle relaxants

Example: suxamethonium

40
Q

What is the importance of acetylcholineesterase?

A
  • physiological
  • pharmacological → reversible inhibition
  • toxicological → irreversible inhibition
41
Q

What are reversible cholinesterase inhibitors?

A
  • diagnostic tests
    • Myasthenia gravis
    • short lasting drug is used
  • therapy of Myasthenia gravis
    • physostigmin, neostigmin → longer lasting drugs
  • eye drops
    • glaucoma
42
Q

What is an example of an irreversible cholinesterase inhibitor?

A

organic phosphate molecules

diisopropyl-flurophosphate (DFP)

43
Q
A
44
Q
A

Biochemistry III (8 decks)

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