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neuromembrane biology > Lecture 14 & 15: exocytosis > Flashcards

Lecture 14 & 15: exocytosis Flashcards

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1
Q

What is exocytosis?

A
  • a form of active transport in which a cell transports molecules (eg neurotransmitters or hormones) out of the cell
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2
Q

what is the 2 step process for exocytosis?

A
  1. docking
  2. fusion
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3
Q

describe the 2 types of pathways that are used for exocytosis

A
  1. Constitutive secretory pathway
    * in all cells,** transport vesicles leave the trans golgi network (TGN) and go to the plasma membrane **
    * they secretory vesicles provide new components for the plasma membrane and components that are designed for secretion eg proteoglycans and glycoproteins of the extracellular matrix
  2. regulated secretory pathway
    * specialised secetory cells use a 2nd pathway - involves proteins stored in secretory vesicles for release at a later stage
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4
Q

How are proteins leaving the golgi network sorted into 3 classes?

A

they are sorted into 3 classes based on their destination

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5
Q

Describe the 3 classes of proteins (based on their destination)

A
  1. mannose 6 phosphate (M6P) is used as a sorting signal to direct proteins to lysosomes
  2. some proteins in specialised secretory cells direct them to the** regulated secretory pathway** (via secretory vesicles)
  3. the** constitutive pathway** is used to deliver proteins that lack specialised signals
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6
Q

Describe the regulatory secretory pathway

A
  • specialised cells store their products in secretory vesicles that are involved in the regulatory secretory pathway
  • proteins aggregate in the ionic environment of the trans golgi network and condense further as the vesicles become more acidic and mature
  • the signal for the initiation of the regulated secretory pathway **involves the binding of a hormone or neurotransmitter to a receptor on membrane ** which causes the cell to exocytose the secretory products
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7
Q

what signal ** initiates** the regulated secretory pathway?

A
  • the binding of a neurotransmitter or hormone onto a receptor of the plasma membrane
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8
Q

What is the ‘full collapse’ method of secretion?

A
  • it was previously thought that secretory vesicles completely merge with the plasma membrane before releasing content
  • the vesicles can then be endocytosed after they release their content
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9
Q

what is the ‘kiss and run’ secretion method for secretory vesicles?

A
  • vesicles can quickly dock and expel their contents without full fusion to the plasma membrane
  • vesicles can then be refilled so each vesicle can undergo multiple rounds of secretion
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10
Q

Describe the kiss and run method for synaptic vesicles

A
  • synaptic vesicles turn over rapidly, instead of returning back to the endosome and cell body - they are refilled with neurotransmitter
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11
Q

what are porosomes?

A
  • they are cupshaped lipoproteins found in the plasma membrane of eukaryotic cells
  • they are the sites** where the secretory vesicles transiently dock** in the process of vesicle fusion and secretion
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12
Q

Describe what happens to the secretory vesicle at the porosome

A
  • the synaptic vesicles dock at the porosome base which develops intravesicular pressure (swell) via the active transport of water through aquaporins
  • the vesicles transiently fuse at the porosome base via the snare proteins and Ca2+
  • they then expel their contents (eg neurotransmitters)
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13
Q

Describe the life cycle of a neurotransmitter

A
  • they are released from the presynaptic nerve terminal
  • they diffuse across the synaptic cleft
  • they bind to receptors on the post synaptic membrane (eg glutamate binds to AMPA)
  • they are then broken down by enzymes or reuptake by transporters to neurons and glia
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14
Q

what 2 key proteins are involved in vesicle filling?

A
  • the vacuolar proton pump
  • neurotransmitter- specific vesicular transporter
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15
Q

what is the role of the vaculolar pump in vesicle filling?

hint : ATP

A
  • it is a multi unit ATPase
  • it creates** transmembrane electrochemical gradient **
  • the electrochemical gradient acts as a energy source for active uptake of transmitter by transporter proteins
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16
Q

what is the role of the neurotransmitter specific vesicular transporter?

A
  • it is an integral membrane protein that transports neurotransmitters
  • 4 types have been identified - one for Ach, one for catecholmines & serotonin, one for glutamate and one for GABA
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17
Q

How does** Ca2+ affect the release** probability ?

A
  • the synaptic vesicles are held in place by Ca2+ sensitive membrane vesicle proteins (VAMPS) eg synapsin I
  • during an AP, intracellular Ca2+ in the axon terminal can rise significantly
  • **elevated Ca2+ levels activate Ca2+-dependent calmodulin kinase **(CAMKII)
  • CAMKII phosphorylates synapsin I which releases the vesicle from the plasma membrane
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18
Q

what is an example of a Ca2+ sensitive vesicle membrane protein (VAMP)?

A
  • synapsin I
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19
Q

what are examples of proteins involved in vesicle release?

A
  • SNARE proteins - eg synaptobrevin is bound to the vesicle membrane
  • syntaxin and SNAP25 are bound to the plasma membrane
  • synaptotagmin - calcium binding protein- when Ca2+ binds to it, the protein binds to the SNARE proteins
20
Q

what is vesicle priming?

A

it is the process that synaptic vesicles must undergo after docking and before fusion

21
Q

what are the main SNARE proteins in the snare complex?

A
  • **VAMPS **(vesicle associated membrane proteins) - eg synaptotagmin & synaptobrevin
  • syntaxin - protein on the plasma membrane
  • SNAP25 - 2 protein strands that bring the vesicle membrane and the plasma membrane together
22
Q

what happens to the SNARE complex after fusion?

A

the snare complex **disassembles **

23
Q

what are examples of pathological** disorders of the NMJ**?

A
  • Myasthenia Gravis
  • Lambert Eaton syndrome
  • Tetanus toxin
  • Botulinium Toxin
24
Q

what kind of disease of myasthenia gravis?

A
  • an auto-immune disease
  • antibodies are produced that are directed against the Ach receptors at the NMJ which decreases the availibility of receptors for binding to Ach
    *
25
Q

what are the** symptoms** of myasthenia gravis?

A
  • long term skeletal muscle weakness
  • most common areas affected are the** eye and eyelid movement, facial expression** &chewing, talking and swallowing
  • more progessive forms can target the respiratory tract, neck and limb movement
26
Q

how could MG symptoms possibly be reversed?

A
  • by using inhibitors of AChe
27
Q

what **structural changes **does MG cause in the NMJ?

A

1.** enlargement** of the synaptic cleft
2. junctional folding is reduced

28
Q

Describe the **mechanism of action **of MG

ie how do the antibodies interact with the receptors?

A
  • the antibodies may bind and cross-link the receptors
  • cross linking of the antibodies to the receptors sends a signal to speed up decomposition by phagocytosis
  • they may trigger receptor recycling by endocytosis
  • lysosomes also involved to help with decomposition
29
Q

Describe the possible causes of MG?

A
  • autoimmune disease
  • bacterial infection- bacterial antigens may share epitopes with the Ach receptors
  • Viral infection -a viral protein may include a peptide sequence that is similar to one in the Ach receptor
  • thymomas- tumours derived from epithelial cells in the thymus - 50 % of patients with these tumours develop MG
30
Q

what are the possible treatments for MG?

A
  • there is** no known cure**
  • lifestyle changes - ie increasing rest periods can help to restore function
    * immunosupressant treatment - reduce and minimize the immune response (ie antibody production)
  • surgical intervention - eg if thymoma was the cause of MG
31
Q

what type of disease is Lambert-Eaton syndrome?

A
  • very rare autoimmune disorder
32
Q

what are the** symptoms** for Lambert-Eaton syndrome?

A
  • muscle weakness in limbs- note has greater impact to legs
  • difficulty in climbing stairs and stand - sit movements
  • difficulty walking
  • in advanced stages of the disease, there can be respiratory difficulties
33
Q

what is the mechansim of action of Lambert-Eaton syndrome?

A
  • antibodies are produced that act against the P/Q type Ca2+ channels in the presynaptic which inhibits neurotransmitter release
  • they bind partcularly to the doman III S5-S6 linker peptide
  • this binding reduces the influx of Ca2+ to the presynaptic terminal
34
Q

what are the possible treatments for L-E-S?

A
  • no known cure
  • immunosupressant treatment- less effective than for other immune conditions eg MG
  • lifestyle changes - aimed at minimising risk of small cell lung cancer eg no smoking,reduce exposure to radiation
35
Q

what are examples of pharmacuetical drugs that can promote the function of the NMJ?

A

*** Amifampridine **- only approved drug treatment for L-E-S, it blocks voltage gated K+ channels and prevents K+ efflux which prolongs the depolarisation and lengthens the action potential duration

36
Q

What is tetanus caused by?

A
  • tetanus is caused by the**tetanus neurotoxin **that is released from infection by Clostridium tetani
  • the endospores of the bacteria live in an anaerobic environment eg soil, manure etc until they find a suitable environment to metabolise and proliferate
37
Q

what are** examples of symptoms** of tetanus?

A
  • symptoms can take up to 3 weeks to occur
  • spasmogenic toxicity
  • begins with the facial muscles - eg lock jaw (muscles of the jaw spasm) and in severe cases it can spread to other areas in the body
38
Q

How does the tetanus toxin enter the NS and how does it travel?

A
  • tetanus toxin enters the nervous system at the NMJ
  • it migrates through the nerve trunks and into the CNS by **retrograde axonal transport **
  • then there is** transcytosis** (transport across the interior of a cell) from the axon into the inhibitory interneurons of the spinal chord
39
Q

what is the mechanism of the actual neurotoxin released in tetanus?

ie what transmitter does the neurotoxin interact with?

A
  • the toxin acts by specifically interfering with glycine release from interneurons in the spinal chord
  • glycine is an **inhibitory transmitter **in the spinal chord which acts on the glycine receptor - which is structurally and functionally similar to the GABA receptor
  • if glycine release is blocked, there is an increase in skeletal muscle activity (ie spasm)
40
Q

what are the treatments for tetanus?

A
  • immunisation with the** tetanus vaccination** - for prevention
    * tetanus antibody Iv infusion or im injection
  • antibiotics might reduce toxin production
  • muscle relaxants to control spasms
41
Q

What is **botulism **caused by?

A
  • caused by the botulinum toxin that is a neurotoxin thats released by Clostridium botulinum
  • the bacteria is mostly found in untreated water or** badly preserved food** eg tinned food
  • can also be through wound infection or intestinal (ie bacterial spores develop in intestines and release toxin)
42
Q

what are the symptoms of botulism?

A
  • begins with muscle weakness
  • blurred vision, speech disruption
  • fatigue
  • paralysis
  • respiratory failure in severe cases
43
Q

what is the **mechanism **of the botulinum toxin?

A
  • there are** eight different toxins** (BT-A to G)
  • botulinum toxin contains heavy and light chains
  • the heavy chain binds to glycoprotein structures that are specifically found on cholinergic nerve terminals
  • after internalisation, the** light chain** of the toxin binds with high affinity to the SNARE complex eg BT-A cleaves SNAP25
  • this **prevents the docking of the Ach vesicle **and therefore **prevents vesicle fusion **and Ach release
44
Q

what are examples of treatments of botulism?

A
  • The key is early diagnosis
  • if it was** food borne** - can treat with induced vomiting to remove contaminated food from gut
  • wound infection- can use surgery to remove the infected material from wound
    * Botulinum antitoxin- removes toxin from blood stream to prevent worsensing of symptoms
  • antibiotics to treat wound infection
45
Q

ewhat are the** therapeutic uses** of the botulinum toxin?

A
  • treatment of disorders with** overactive muscle movement** eg cerebral palsy
  • treatment of** excess sweating or salivation**
  • migraines

neuromembrane biology (14 decks)

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