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M2-2 > NTMetabolism > Flashcards

NTMetabolism Flashcards

1
Q

Otto Lowei’s experiment (Step and Findings)

A

Step
1. Stimulate vagus of donor heart (frog); heart rate slow down as a response
2. Remove fluid sample
3. Add fluid to the recipient heart
Finding
1. The recipient heart rate slowed down too
2. Atropine can bring back the heart rate (meaning it is not a damage)
3. First discovery of NT!

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2
Q

What is a NT?

A
  1. Released by the nerve ending of a neuron that is used to communicate with the adjacent neuron.
  2. Cause response on post synaptic neuron (excite or inhibit)
  3. Quickly degraded in the synaptic cleft, diffuse or taken up by the presynaptic neuron
  4. Block of action is possible by antagonist or blocking the synthesis
    e. g. Serotonin, Acetylcholine, Dopamine, GABA, Glycine, and Norepinephrine
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3
Q

What is a neuromodulator?

A
  1. Released by the nerve endings and have their effect sometimes quite FAR from the neuron from which they were released.
  2. They can either dampen or enhance the excitability of their effector neurons.
  3. They are NOT rapidly degraded or taken up.
    e.g. opioid peptides such as enkephalins, endorphins, dynorphins.
    Some NT also act as neuromodulators: substance P, octopamine, serotonin, and acetylcholine
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4
Q

Limitation of classical definition of NT

A
  1. Direction of pre->post synapse:
    retrograde messengers, presynaptic autoreceptors
  2. Ion channels vs metabotropic cascade:
    Ach, Glu, GABA have both though metabotropic is more regarded as neuromodulators not NT
  3. Limited extracellular lifetime:
    Some NTs have tonic substance concentration
  4. Defined pharmacology:
    Difficulty of truly replicating the study e.g. are we sure there are no artefacts/human errors/contamination?
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5
Q

What type of biomolecule exist?

A 
Building block -> larger unit of cells
Sugars -> polysaccharides
Fatty acids -> fats, lipids and membranes
Amino acids -> proteins
Nucleotides -> nucleic acids
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6
Q

Biomolecule and its orders

A

“low” order
- sugars (carbohydrates)
- peptides
- lipids
- heterocyclic compounds
“medium” order
- nucleotides (ATP, GTP, NADPH, FADPH, DNA and RNA bases)
- peptides (opiates)
“high” order
- proteins ( can contain peptides, sugars, FA)
- DNA, RNA (contains nucleotides, phosphate esters)

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7
Q

Which order of molecule is important for cellular metabolism

A

medium

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8
Q

What is glycolysis?

A

Conversion of glucose to pyruvate

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9
Q

What is the outcome of TCA cycle?

A

Acetyl CoA -> cycle -> ATP/GTP, NADH, FADH

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10
Q

Acetyl CoA

A

= pyruvate + FA

building blocks for most molecules; universal donor of C atoms

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11
Q

Purinergic system

A

Released: Activity (Ca2+) dependent manner
Conversion: ATP -> ADP -> AMP
Receptors:
classical fast neurotropic (ligand gated) channels and metabotropic (g-coupled) R
both in pre (Na+ dependent N1 transporter) and post 4 GPCR for adenosine, 1 ligand and 1 GPCR for ATP

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12
Q

Purinergic receptors

A

Adenosine and ATP are NT with specific receptors
Adenosine have 4 GPCR (A1, A2a, A2b, A3)
ATP have ligand gated (P2X) and GPCR (P2Y)

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13
Q

ATP profile

A

Source: Acetyl CoA -> TCA cycle
Enzyme: -
Storage: Together with ApnA
Inactivation: Degenerated to Adenosine

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14
Q

How is Adenosine produced and deactivated?

A

ATP -> ectodiphosphohydrolase -> ecto5 nucleotidase -> Adenosine (Ado)
Ado can then
- activate GPCR on pre and post (A1)
- activate GPCR on post (A2) -> excite/inhibit cAMP pathway
- recycled to pre via Na+ dependent transporter

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15
Q

What is a lipid rafts

A

Cholesterol rich patches of cell membrane forming a distinctive microenvironment, making the cross phosphorylation easier

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16
Q

How does fatty acid play a role in binding?

A

Fatty acids (-COOH) can be posttranslationally attached to molecules, this anchor allows the monomers to stay in place (creating lipid raft, thus enhancing the signalling cascade)

17
Q

How is P2Y activated?

A

By fatty acids posttranslational modification

ATP bind -> activated PIP3 kinase -> PIP activated -> docked intracellular signalling protein activated -> relay signal

18
Q

What are some prominent lipids?

A

TetraHydroCannabinol, Anandamide(type of body-produced endocannabinoid), Prostaglandin E1, Cholestrol and its derivatives (cortisol, estradiol, testosteronevitamin D3, )

19
Q

How is Endocannabinoid Signalling different?

A

Excessive stimulation of inhibitory cells -> less signalling -> less inhibition (Depolarization induced Supression of Inhibition)
Possible explanation for epilepsy
EC signalling is atypical because it signals backwards from post to pre! The act as retrograde messengers, suppressing presynaptic release of inhibitory transmitters

20
Q

What are the steps for Endocannabinoid Signalling?

A

Pre: Inhibitory cell
Post: cannabinoid secretory cell
1. Trigger signalled by intracellular Ca2+ elevation and mGluR activation of postsynaptic cell
2. Depol of post synaptic cell by swamping with Glutamate and Ca2+
3. Leads to production of EC ”on the fly/on spot”
4. EC get secreted from post and binds to pre
5. Binding activates the g protein leading to inhibition of 6. Ca influx to pre
Pre synaptic release is decreased

21
Q

Pathway 1: Anandamide (EC) breakdown

A 
Phosphatidylethanolamine
-(N-acyltransferase*)->
N-arachidonoyl PE
-(Phopholipase D*) ->
Anandamide
-(Fatty Acid Amide Hydrolase)->
arachidonic acid + ethanolamine
*Ca dependent enzyme
22
Q

Pathway2 : 2-AG (EC) breakdown

A 
Phosphatidylinositol (PI)
-(Phospholipase Cb*)->
Diacylglycerol
-(DAG lipase)-> 2 Arachidonylglycerol (2-AG)
-(MonoacylGlycerol Lipase)
-> Arachidonic acid + glycerol
*Ca dependent enzyme
23
Q

What deactivates cannabinoid?

A 
FAAH (anandamide) and MGL (2AG)
Anandamide
-(Fatty Acid Amide Hydrolase)->
arachidonic acid + ethanolamine
2 Arachidonylglycerol (2-AG)
- (MonoacylGlycerol Lipase)
-> Arachidonic acid + glycerol
24
Q

EC profile

A 
Source: Phosphatidylethanolamine 
 (Anandamide) and Phosphatidylinositol(2AG)
Enzyme: Phopholipase D and DAG lipase
Storage: - 
Inactivation: FAAH and MGL
25
Q

What’s special about sugar?

A

Only sugars do NOT act as NT/neuromodulators on its own

26
Q

Storage to NT outlier

A

Neuroactive peptides are sorted differentially compared to the classical NT

27
Q

Example of biomolecule and its neuroactives

A

AA: Glycine, Glutamate, Dopamine
Protein (AA): BDNF, NPY, NPS, Insulin, Opioid
FA: THC, EC
Nucleotide (FA): ATP, Adenosine

M2-2 (10 decks)

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