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Neuro Block 2 - KJ > NT Metabolism > Flashcards

NT Metabolism Flashcards

1
Q

What is the active ingredient in L’absinthe and what does it do?

A

Thujone
-Causes blocking of the GABAa receptor [Cl- channel antagonist/blocker] –> inhibits inhibitor causing potential muscle spasms and convulsions

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2
Q

What are the detailed steps in the process of NT transmission?

A
  1. Packaging - NT is synthesized and then stored in vesicles
  2. An AP invades presynaptic terminal
  3. Depolarization of presynaptic terminal causes –> opening of VG Ca++ channels
  4. Influx of Ca++ through channels
  5. NT is released into synaptic cleft via exocytosis
  6. NT binds to receptor molecules in postsynaptic membrane
  7. Opening or closing of postsynaptic channels
  8. Postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell
  9. Removal of NT by glial uptake or enzymatic degradation
  10. Retrieval of vesicular membrane from plasma membrane
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3
Q

What are some general steps in the process of neurotransmission?

A 
Presynaptic cell
1. NT synthesizing enzymes
2. Synaptic vesicle transporters
3. Reuptake transporters
4. Degradative enzymes
Postsynaptic cell
5. Transmitter-gated ion channels
6. G-protein coupled receptors
7. G-proteins
8. G-protein gated ion channels 
9. Second messenger cascades
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4
Q

What are the two chemical messenger types (NT)?

A
  1. Biogenic Amines

2. Neuropeptides (Opioids, Oxytocin, Glucagon, growth hormone releasing hormone, etc.)

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5
Q

What four properties does a NT need?

A
  1. Present at nerve terminal
  2. Should be released
  3. Should be a receptor for it [NT receptors activated]
  4. Response should be blocked or activated [application of transmitter agonists or antagonists]
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6
Q

How are small molecules (amines) produced?

A

Made in pre-synaptic zone, enzymes that make these are made in nucleus and carried down by dyenins etc.

  1. Synthesis of enzymes in the cell body
  2. Slow axonal transport of enzymes
  3. Synthesis and packaging of NT at terminal
  4. Release and diffusion of NT
  5. Transport of precursors into terminal
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7
Q

How are peptides produced?

A

Synthesized near nucleus/top and then put on railroad track down to cell terminal

  1. Synthesis of NT precursors and enzymes (nucleus)
  2. Transport of enzymes and peptide precursors down microtubule tracks
  3. Enzymes modify precursors to produce peptide NT
  4. NT diffuses away is degradated by proteolytic enzymes
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8
Q

What is the process of synaptic vesicle recycling at presynaptic terminals?

A
  • Process happening every minute
  • Budding (from endosome) –> Docking –> Priming –> Fusion –> Budding (of vesicle back into presynaptic nerve terminal and fusing into endosome)
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9
Q

What vesicle membrane proteins are involved in docking, attaching and releasing vesicle contents?

A

SNAP 25, Synaptobrevin, Syntaxin

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10
Q

What vesicle membrane proteins are transporters that take NT and pump it against its conc. gradient?

A

V-ATPase & VGLUT

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11
Q

What are SNARE proteins?

A
  • Proteins involved in docking and fusion

- v-SNAREs and t-SNAREs

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12
Q

What does Clostridium sps. do to neurotransmission?

A
  • It produces zinc proteases that hydrolyze proteins (SNAREs) so that vesicles cannot dock properly & NT will be stopped
  • In brain = this may lead to seizures
  • In spinal cord = may lead to paralysis
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13
Q

What does black widow spider venom do? What is is called?

A

Alpha-latrotoxin

  • Causes fusion to occur in the absence of Ca2+
  • Already releasing NT without an AP
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14
Q

What does tetanus and botulinum toxin do?

A

Affect SNARE proteins involved in vesicle fusion

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15
Q

How is acetylcholine made?

A

Acetyl CoA + Choline (choline acetyltransferase) –> acetylcholine

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16
Q

How is acetylcholine broken down?

A

Acetylcholine + H2O (acetylcholine esterase) –> Acetate + Choline

17
Q

What can block ACh’s nicotinic receptor?

A

Curare

-Both ACh and nicotine stimulate this receptor

18
Q

What can block ACh’s muscarinic receptor?

A

Atropine

-Both ACh and muscarine are inhibitory here

19
Q

What happens when an ACh receptor is blocked?

A

No neurotransmission

20
Q

What is a situation where auto-antibodies are produced to AChR?

A

Myasthenia Gravis –Blocks/reduces Neurotranmission (loss of ACh system when you make auto-antibodies against them!)

21
Q

Can acetylcholine breakdown be inhibited?

A

Yes - by Organophosphate which binds to acetylcholinesterase

22
Q

Why do soldiers take an antagonist for ACh receptors?

A

Chemical warfare agents cause too much ACh to bind to your receptors

23
Q

How is glutamate synthesized and cycled?

A
  1. Glutamate is inactivated by being taken up by Glial cells
  2. In glial cell glutamine synthetase produces glutamine
  3. Glutamine travels through EATT o nerve presynaptic terminals
  4. Glutaminase converts glutamine to glutamate
  5. Glutamate is packaged through VGLUT into vesicles for release
24
Q

What receptors are very fast?

A

Glutamate!! (ms)

  • Na+ channels
  • AMPA receptor
  • NMDA (Ca2+) receptor
  • Kainate receptor
25
Q

What receptors are very slow?

A

Second-messenger linked receptor (GPCR) (sec-hr)

-Quisqualate B

26
Q

How does stroke/excitotoxicity/epilepsy/trauma cause cells to die?

A

Too much Ca2+ influx = bad!

  • All of the ions in the cell cause water to flow in and cells die
  • Overstimulation of neurons during seizures cause great glutamate release at synapses –> Inc. in intracellular Ca2+ –> CaMK11, NOS, Proteases –> Mitochondrial & Nuclear damage –> Necrosis or Apoptosis [Na+ influx leads to Cl- influx –> water swelling/cell lysis]
27
Q

How are GABA and Glycine (amino acids) metabolized?

A
  1. Glial cells take up GABA/deactivate it, give off GABA through GAT and GABA is broken down in the terminal into glucose
  2. Glucose is used to make Glutamate
  3. Glycine goes through a similar cycle [except glucose becomes serine which processed by serine hydroxy-methlytransferase to make Glycine
28
Q

How are biogenic amines synthesized?

A

Tyrosine –> eventually –> Dopamine –> Norepinephrin –> Epinephrine
Tryptophan –> Serotonin

29
Q

How are biogenic amines inactivated?

A

High affinity:
1. Monoamine uptake transporters have high affinity for certain monoamines more than others but may take others
2. Biogenic amines are inactivated PRIMARILY by repute into the presynaptic terminal ends (near terminal but not at site)
Low affinity:
1. Organic Cation Transporter & Plasma monoamine transporter –> present on neighboring cells but remove less monoamines

30
Q

What are the biogenic amines? How are they degraded/excreted?

A

-Dopamine, Norepinephrine, Epinephrine
First they are inactivate and then excreted through urine
Dopamine –> Homovanillic acid (HVA)
Norepinephrine –> 3-methyl-4-hydroxymandelic acid

31
Q

How do endocannabinoids/marijuana drugs transmit signals?

A

Retrograde messengers

32
Q

How do retrograde messengers work?

A
  1. Made/synthesized at postsynaptic cell
  2. Diffuse to presynaptic terminal
  3. Acts to cause vesicles to dock in presynaptic cell and release NTs
33
Q

What are the endocannabinoids?

A
  • Anandamide
  • 2-arachidonylglycerol (2-AG)
  • Delta-9-THC
34
Q

Where do endocannabinoids work?

A
  • Substantia nigra
  • Cerebellum
  • Hippocampus
  • Caudate putamen

Neuro Block 2 - KJ (14 decks)

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