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Year 2 - Theme 1 > Chemicals in the brain part 2 > Flashcards

Chemicals in the brain part 2 Flashcards

1
Q

What are the monoamines

A
  • Catecholamines - dopamine, epinephrine(adrenaline) and norephinephrine
  • Indolamines - serotonin(5-Hydroxytryptamine, 5-HT)
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2
Q

What are the two steps of dopamine synthesis

A

1) Tyrosine –> L-dopa reaction carried out by Tyrosine hydroxylase
2) L-dopa –> dopamine reaction carried out by dopa decarboxylase

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3
Q

What is administered for treating parkinson’s disease

A
  • Levodopa
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4
Q

How is epinephrine synthesised

A
  • Dopamine –> Norepinephrine carried out by dopamine beta-hydroxylase(DBH)
  • Norepinephrine –> epinephrine carried out by phentolamine N-methyltransferase(PNMT)
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5
Q

Location of DBH

A
  • DBH located in synaptic vesicles only, and NE is the only neurotransmitter synthesised within vesicles
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6
Q

How does catecholamine release occur

A
  • Released by Ca2+ dependent exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient(dopamine transporters DATs), norepinephrine transporters(NETs) etc
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7
Q

How does catecholamine reuptake occur

A
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs), Norepinephrine transporters (NETs) etc
    • In the cytoplasm, the catecholamines are
    • Reloaded back into vesicles
    • Enzymatically degraded by monoamine oxidases(MAOs)
      Or
    • Inactivated by Catechol-O-methyl-transferase (COMT)
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8
Q

Effect of amphetamine on catecholamine transporter

A
  • Amphetamine reverses transporter so pumps out transmitter and blocks reuptake(DA and NE)
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9
Q

Effect of cocaine and methylphenidate on DA uptake

A
  • Cocaine and methylphenidate(ritalin) block DA reuptake into terminals
  • More DA in synaptic cleft - extended action on postynaptic neuron
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10
Q

Effect of selegiline on dopaminergic nerve terminals

A
  • MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations(treatment of early-stage PD, depression and dementia)
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11
Q

Effect of entacapone on catecholamine release and reuptake

A
  • Catechol-O-methyl-transferase(COMT) inhibitor

- Treatment of PD

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12
Q

Stages of serotonin synthesis

A
  • Tryptophan –> 5-HTP carried out by tryptophan hydroxylase
  • 5-HTP –> 5-Hydroxytryptamine(Serotonin, 5-HT) carried out by 5-HTP decarboxylase
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13
Q

How does serotonin storage, release and reputake occur

A
  • Stored in vesicles
  • Signal terminated by reuptake by serotonin transporters(SERTs) on presynapticmembrane
  • Destroyed by MAOs in the cytoplasm
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14
Q

Effect of fluoxetine(prozac) on serotonin release and reuptake

A
  • Fluoxetine(prozac) blocks reuptake of serotonin(SSRI - selective serotonin reuptake inhibitor) (treatment of depression, OCD)
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15
Q

Effect of fenfluramine on serotonin release and reuptake

A
  • Fenfluramine stimulates the release of serotonin and inhibits its reuptake(has been used as an appetite suppressant in the treatment of obesity)
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16
Q

Effect of MDMA(methylenedioxymethamphetamine)(ecstasy) on NE and serotonin transporters

A
  • Causes NE and serotonin transporters to run backwards releasing neurotransmitter into synapse/extracellular space/extracellular space(assessed for therapeutic potential in PTSD)
17
Q

What does choline acetyltransferase cause

A
  • Conversion of choline + acetyl CoA into acetylcholine
18
Q

What is acetylcholine packed by

A
  • Is packaged into vesicles by vesicular acetylcholine transporter(VAChT)
19
Q

What is Ach degraded by

A
  • Rapidly degraded in synaptic cleft by acetylcholinesterase(AChE)
  • Acetylcholine –> acetate + choline
20
Q

What happens to choline that is produced from Ach degradation

A
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
21
Q

What is the rate limiting step in acetylcholine production

A
  • Amount of choline is rate limiting step
22
Q

Effect of AChE inhibitors

A
  • Block the breakdown of Ach, prolonging its actions in the synaptic cleft
23
Q

Effect of neostigmine on Ach

A
  • Is an acetylcholinesterase inhibitor which prolongs the action of Ach in the synaptic cleft
24
Q

Effect of black widow spider venom on Ach release

A
  • Stimulates its release
25
Q

Effect of tetanus toxin on the release of glycine and GABA at inhibitory neurons

A
  • Inhibits release of glycine and gABA at inhibitory neurons, resulting in dis-inhibition of cholinergic neurons(release of Ach), which causes permanent muscle contraction
26
Q

What are some examples of neuropeptide transmitters

A
  • Endorphins, neuropeptide y, substance p, endogenous opioids, vasopressin
27
Q

How are neuropeptide transmitters released

A
  • Follow the secretory pathway but NOT released in the same way as small molecule transmitters
  • Dense core vesicle fusion and exocytosis occurs as a result of global elevations of Ca2+(sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
28
Q

How are neuropeptide signals terminated

A
  • Bind to and activate receptor
  • Neurpeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
  • Release is slower than small molecule release and signals may be maintained for longer
29
Q

How does retrograde signalling work with soluble gases such as nitric oxide and carbon monoxide

A

1) Nitric oxide made in postsynaptic neuron by nitric oxide synthase(activated by the binding of Ca2+ and calmodulin)
2) The gas is not stored but rapidly diffuses from its site of synthesis. Diffuses between cells(into presynaptic cell - retrograde transmitter)
3) Activates guanylyl cyclase which makes the second messenger cGMP
4) Within a few secs of being produced, NO is converted to biologically inactive compound(switching off the signal)
5) Useful for coordinating activities of multiple cells in a small region(tens of micrometers)

30
Q

What are some other examples of transmitters/retrograde signalling

A
  • Endocannabinoids - small lipids which cause reduced GABA release at certain inhibitory terminals
  • A cannabinoid is also the active component of the active compoent of marijuana(cannabis sativa)

Year 2 - Theme 1 (30 decks)

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