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Final Biochemistry > Cholinergic Neurotransmission > Flashcards

Cholinergic Neurotransmission Flashcards

1
Q

Where do we find Cholinergic Neurons?

A
  • Neuromuscular junction
  • Autonomic preganglionic Neurons
  • Parasympathetic postganglionic fibres (heart,glands,smooth muscle)
  • CNS
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2
Q

Steps in Cholinergic Nerve Axon Terminal

A
  1. High affinity uptake of Choline
  2. ACh synthesis
  3. Uptake of ACh into vesicle (storage)
  4. Exocytosis of ACh
  5. ACh inactivation
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3
Q

High Affinity uptake

A

Na+,Choline - symporter.

  • dependent on Na and Cl.
  • normal [Choline] plasma —> 10mM
  • km > 10mm so in normal tissues LOW affinity
  • This transport, Km is 1-5mM. THUS HIGH AFFINITY
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4
Q

What is the Choline uptaker inhibited by?

A

-Hemicholinium

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5
Q

synthesis of ACh

A

Done by —> Choline Acetyltransferase.

  • cytoplasmic
  • NOT rate limiting
  • used for immunohistochemical mapping of cholinergic neurons.
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6
Q

Uptake of ACh into vesicles?

A

Done by —> Vesicular ACh Transporter (VAChT)

-
-H+,ACh antiporter.

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7
Q

What is VAChT inhibitted by?

A

-Vesamicol

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8
Q

What triggers the exocytosis of ACh vesicles?

A

AP -> Depolarisation of Neurons -> Ca2+ entry via VDCC –> exocytosis of vesicles.

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9
Q

Steps in Exocytosis of Synaptic Vesicles

A
  1. uptake of neurotransmitter into vesicle.
  2. formation of reserve pool - clumping of vesicles.
  3. Docking of vesicles onto active zone.
  4. Priming - vesicle becomes competent for Ca++ signal.
  5. Ca++ signal - fusion pore opens.
  6. Vesicle recyling:
    • kiss and stay : ->refilling w/o undocking
    • Kiss and run : ->vesicle releases NT and returns
    • full endocytosis
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10
Q

Docking

A

SNARE and Synaptotagmin not involved.

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11
Q

Priming

A

SNARE complex forms on vesicle.

Synaptotagmin become associated with complex.

Vesicle and plasma are in close proximity - forming unstable intermediate.

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12
Q

Fusion

A

Ca++ signal -> Synaptotagmin C2 domain inserts into phospholipid membrane.

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13
Q

What are SNARE’s receptors for?

A

NSF (N-ethylmaleide Sensitive Factor) and NSF soluble factors.

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14
Q

SNARE in Synaptic Vesicle

A
  • VAMP (vesicular Associated membrane protein)

- Synaptobrevin

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15
Q

SNARE in plasma membrane

A
  • Syntaxin 1 A/B

- SNAP-25 (synaptosomal-associated protein)

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16
Q

Energy for fusion of vesicles

A

-Done by the sponatenous formation of a-helices in the cytosol by SNARE motiffs.

-These a-helices become supercoiled and parallel coiled structures.
This provides the energy

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17
Q

How many AA in SNARE proteins

A

70 AA homolog sequence (SNARE motiff)

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18
Q

Fusion-core complex:

A

parallel helices are formed with the SNARE sequences that span into the cytosol (four sequences from three proteins).

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19
Q

What is the Ca++ sensor?

A

Synaptotagmin!

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20
Q

Regulatory proteins involved in Exocytosis

A
  • Munc18-1
  • Complexis
  • Synaptophysins (vesicular)
  • Synapsins (vesicular)
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21
Q

v-snares

A
  • Synaptobrevin

- VAMP

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22
Q

T-snare

A
  • Syntaxin 1 A/B

- SNAP-25

23
Q

formation of fusion pore after Ca2+ signal

A
  1. T-snare + V-snare bind.
    They begin to zip from the N-terminal. Bringing membranes close to one another.

2.Zipping causes ->lateral tension on PM
curving of PM
hemifusion of the outer layers

  1. Hemifusion of the inner layers
  2. complete fusion causes pore complex
  3. contents emptied out
24
Q

Structure of Botulinum Toxins

A

Heavy Chain and Light chain

25
Q

How is Botulinum toxins taken up into the Cholinergic Neurons

A

-Acceptor mediated Endocytosis.

26
Q

How does Botulinum affect Cholinergic Neurons

A

-Inhibits Exocytosis with LC (Catalytic domain).

  • -> Zn2+ - dependent endproteases
  • -> has specificity for sites in the SNARE Protein
27
Q

affect of Botulinum Toxins on SNARE complex stability

A

Botulinum either increases or decreases the stability of SNARE.

28
Q

Types of Cholinergic Receptors

A

1) Muscarinic

2) Nictonic

29
Q

Where do we find Muscuranic receptors

A

Organs innervated by:

  • > Parasympathetic postganglionic
  • > CNS
30
Q

Where do we find Nicotonic receptors?

A

Neuromuscular junction

31
Q

Inhibitor of Muscuranic receptor

A

Atropine

is a competitive inhibitor

32
Q

Inhibitor of Nictonic receptor

A

Crurae

33
Q

Molecular mechanism of Muscuranic receptors?

A
  1. PLC activation
  2. [Ca]i Increase
    3) inhibition of Adenyl Cyclase
    4) Activation of K+ channels
34
Q

Molecular mechanism of Nictonic receptors

A

Na+ and K+ channels

35
Q

M1 receptor

A
  • 7 transmembrane protein
  • Gq coupled

-PLC —> PIP2 Hydrolysis –> IP3 —> Ca signal

36
Q

M2 receptor location

A

M2 receptors are found in the heart

37
Q

Which G-protein is M2 receptors coupled with?

A

Gi

  • K+ channel activation—> HYPERPOLARIZATION –> BRADYCARDIA
  • inhbition of cAMP
  • inhibition of Ca++ signal
38
Q

M3 receptor location

A

Gastro-intestinal tract

39
Q

M3 receptor coupled G-protein

A

Gq

40
Q

M3 receptor effects

A
  • Smooth muscle contraction

- secretion stimulation

41
Q

Muscle Type Nictonic Receptor

A
  • In striatal muscle
  • has Na+ and K+ permeability.
  • causes membrane depolarisation which leads to Ca++ release from SR.
42
Q

What is muscle type nictonic receptor inhibitted by?

A

D-Tubocuranine (competitive inhinb)

43
Q

How many subunits in Nictonic receptors

A

5.

  • A x 2 (binding site of ACh)
  • B
  • D
  • G
44
Q

Inhibitors of Nictonic receptors

A
  • > > > D-tubocruranine:
  • comp inhibitor

-»>a-bungarotoxin:

  • from a indian
  • SPECIFIC for muscular Nictonic receptors
45
Q

Events following the stimulation of nicotinic receptors in skeletal muscle

A
  1. Neurotransmitter released diffuses across the synapse and binds to the Nictonic receptors on the sarcolemmma.
  2. Causes depolarisation and AP propagates down the T-tubules.
  3. Causes release of Ca++ from cisternae of SR
  4. Ca++ binds to Trop-C causes change of shape, which pulls Tropomyosin off the actin.

etc etc

46
Q

What is Malignant Hyperthermia

A

-rare complication during inhalation of anaesthia due to genetic defect in ryanodine receptors.

47
Q

What happens in Malignant Hyperthermia

A
  1. Mutated Ryanodine receptor.
  2. Altered kinetics of Ca++ channels.
  3. Persistent large increase in [Ca++]i

causes:

  • –> HYPER METABOLISM (fever)
  • –> Persistent activation of the muscle (muscle ridgity)
48
Q

Acetylcholine Esterase - facts

A
  • Located in the synapse.
  • Specific for ACh
  • It is a serine protease
49
Q

Mechanism of Acetylcholine esterase

A
  1. ACh binds to active site of enzyme.
  2. Choline released and we have Acetyl-Enzyme complex.
  3. Hydrolysis of the complex to form -> ACETATE , H+ and Acetylcholine Esterase.
50
Q

Pseudocholinesterase

A
  • found in Plasma and Liver.
  • function is UNKNOWN BUT

we think it involved in:

->hydrolysis of other esters (acting as short-term muscle relaxant).

51
Q

effects of: –> suxamethonium

A
  • It is a Nic ACh receptor agonist.

- causes muscle relaxation and temporary paralysis.

52
Q

Reversible inhibitors of Acetylcholine esterase

A
  • have a pharmalogical use.

examples: 1) Physostigmin 2) Neostigmin

53
Q

Disease which is treated with reverisble acetylcholine esterase

A
  • Myasthenia Gravis
  • we use short lasting drug to test.
  • physostigmin and neostigmin are long loasting.
  • eye drops used for glaucoma.

Final Biochemistry (5 decks)

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