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Neurobiology > Biogenic Amines > Flashcards

Biogenic Amines Flashcards

0
Q

Give example of an indolamine

A

Serotonin

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1
Q

Give examples of catecholamines

A

Dopamine
Noradrenaline
Adrenaline

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2
Q

Give example of an imidazoleamine

A

Histamine

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3
Q

How is dopamine synthesised ?

A

Tyrosine to L-dihydroxyphenylalanine by tyrosine hydroxylase
L-dihydroxyphenylalanine to dopamine by dopa decarboxylase

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4
Q

Is tyrosine an essential or non essential amino acid ?

A

Non essential but we still take it in in our diet so there’s a plentiful supply of it

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5
Q

What does alpha- methyl-p-tyrosine do ?

A

Inhibits tyrosine hydroxylase
It’s used as a research tool but not clinically because if it is given clinically then you wouldn’t be able to produce any of the catecholamines

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6
Q

What is the rate limiting step in dopamine synthesis ?

A

Tyrosine hydroxylase

L-dopa can be given to bypass this rate limiting step

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7
Q

What drug if administered alongside l-dopa in the treatment of PD and why ?

A

Carbidopa
Because L-dopa can be converted to dopamine in the periphery but we want it in the brain and dopamine can’t cross the BBB but L-dopa can so the carbidopa blocks periphery dopa decarboxylase

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8
Q

Where is dopamine within neurons ?

A

Some is stored in ready releasable pools - use VMAT transporter to put dopamine into vesicles
Some is just present in the cytosol
Some is in long term storage - in vesicles just further back from the active zone

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9
Q

What happens to dopamine once it’s released ?

A

1- some binds to pre and post synaptic receptors
2- some diffuses away from the cleft
3- some is taken back up into the terminal by a specific dopamine transporter

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10
Q

What are the dopamine receptors ?

A

Metabotropic
D1-D5
2 families : D1 like (1 and 5) and D2 like (2,3 and 4)

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11
Q

How do D1 like receptors work ?

A 
Linked to Gs
Activate adenylate Cyclase 
Increase cAMP 
Increase pKA 
Proton phosphorylation
Eg inhibits GIRK to cause depolarisation
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12
Q

How do D2 like receptors work ?

A

Linked to Gi
Inhibit adenylate Cyclase
Decrease cAMP
Decrease pKA and protein phosphorylation
EF cause opening of potassium channels causing inhibition
These are the most important ones for drug therapy but most drugs are not selective

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13
Q

How is dopamine reuptaken ?

A

Taken up by specialised transporter - reducing its effects

It is a probable site for drug action

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14
Q

What do amphetamines do ?

A

Block uptake transporter and increase levels of dopamine in the synaptic cleft
Also reverses the transporter to increase the release of dopamine from the cytosol

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15
Q

How does cocaine work ?

A

Blocks dopamine up take transporter so enhances dopamines effects

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16
Q

What are 2 examples of therapeutic dopaminergic drugs ?

A

Benzhexol and amantadine

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17
Q

What is cocaine ?

A

Alkaloid found in leaves of South America shrub erthroxylon coca
Powerful psychostimulant
Acts of dopaminergic pathways involved in reward
Primarily blocks reuptake in the midbrain causing exhilaration

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18
Q

What are amphetamines ?

A

Synthetic compound
Psychomotor stimulant
Many sympathomimetic effects
Inhibits uptake of catecholamines and inhibits mono amine oxidase so stops them being broken down

19
Q

What are the 2 pathways involved in dopamine catabolism ?

A

Monoamine oxidase - 90%

Catechol-o-methyltransferase -10%

20
Q

Describe the MAO catabolism pathway for dopamine.

A

Dopamine to 3,4-dihyroxyphenylacetylaldehyde by MAO
3,4-dihydroxyphenylacetylaldehyde to 3,4-dihydroxyphenylacetic acid by aldehyde dehydrogenase
3,4-dihydroxyphenylacetic acid to homovanilic acid by COMT

21
Q

Describe the COMT pathway to catabolise dopamine

A

Dopamine to 3-methoxytyramine by COMT
3-methoxytyramine to 3-methoxy-4-hydroxy-phenylacetylaldehyde by MAO
3-methoxy-4-hydroxyphenylaldehyde to homovanilic acid by aldehyde dehydrogenase

22
Q

Where is MAO found ?

A

In membrane of mitochondria
2 types a and b
Dopamine metabolised by both

23
Q

What happens to dopac and hva ?

A

Dopac can be eliminated directly whereas hva is eliminated in the CSF

24
Q

What is an example of a MAO inhibitor ?

A

Phenelzine

25
Q

Which 2 areas of the brain are dopaminergic cell bodies clearly visible ?

A

Substantia nigra pars compacta
Ventral tegmental area
They are both nuclei of the midbrain

26
Q

Why is the substantia nigra black?

A

Due to high levels of melanin

27
Q

What are the 3 dopaminergic pathways from the midbrain to telencephalon areas ?

A

Nigro-striatal = substantia nigra to striatum to putamen to cortex for initiating movement
Mesocortical and Mesolimbic pathways from ventral tegmental area

28
Q

What are the 4 interconnected subcortical nuclei of the basal ganglia ?

A

Substantia nigra
Subthalamic nucleus
Striatum
Globus pallidus

29
Q

What is the cell group name of the dopaminergic neurons in the substantia nigra ?

A

Neuronal cell group A9

Terminate in the striatum which is made up of the caudate nucleus, putamen and ventral striatum

30
Q

What is the mesocortical pathway ?

A

Arises from ventral tegmental area -A10
Innervates hippocampus, amygdala, septum, prefrontal cortex and other limbic systems
Important in higher cortical functions such as memory, emotion and thought

31
Q

What is the Mesolimbic pathway ?

A

Arises from the ventral tegmental area
Innervates the nucleus acumbens and olfactory tubercle
Important in arousal, locomotor activity, reward, motivation and affective States

32
Q

How is noradrenaline synthesised ?

A

Dopamine to noradrenaline by dopamine beta-hydroxylase
This enzyme is only found in noradrenergic neurons
Noradrenaline is only produced inside vesicles not in cytosol

33
Q

How is adrenaline made ?

A

Noradrenaline to adrenaline by phentolalanine methyltransferase -PNMT
PNMT is mainly found in adrenal medulla

34
Q

How is noradrenaline stored ?

A

In synaptic vesicles
Put into them by transvesicular proton gradient
Reserpine can block this transporter

35
Q

What did reserpine use to be used to treat and why is it no longer used ?

A

Use to be used to treat hypertension because it blocked the release of noradraline which causes vasoconstriction of blood vessels
But it meant that no noradrenaline was released and this caused high incidence of depress,ion and suicide

36
Q

What are the adrenoreceptors ?

A

Alpha (1+2) and beta (1+2+3)

GPCRs

37
Q

How do alpha-1 receptors work ?

A

Activate phospholipase c
Increase IP3 and DAG
Increase intracellular calcium
Inhibits potassium leak channels and causes EPSP

38
Q

How do alpha-2 receptors work ?

A

Inhibit adenylate Cyclase
Decrease cAMP
Activates voltage gated potassium channels and cause IPSP

39
Q

How do beta- receptors work ?

A

Activate adenylate Cyclase
Increase cAMP
Close potassium leak channels and cause EPSP

40
Q

Where are noradrenergic neurons in the brain ?

A

Mainly localised to the locus coerulus in the pons/medulla and reticular formation.
Axons from locus coerulus project rostrally to almost all brain area
Are descending axons to spinal cord and brain stem

41
Q

What colour does the locus coerulus appear and why ?

A

Blue due to the large amount of noradrenaline

42
Q

What are the functional roles of noradrenergic neurons ?

A

Arousal and mood - cells in lc implicated
Blood pressure regulation -synapses in medulla are part of baroreceptor reflex
Wakefulness and alertness -

43
Q

What are th effects of noradrenaline release in the CNS?

A

Predominately a neuromodulator
Modulates inhibitory and excitatory inputs
Reduces firing rates in the cerebellum, cochlear nuclei and auditory cortex but increases their excitation by afferent innervation

44
Q

How many amino acids make up the D1 receptor?

A

446
3rd and 5th domains and extracellular loop that bind dopamine
Intracellular 3rd loop interacts with Gs protein

45
Q

What do the D2 receptors often act as ?

A

Autoreceptors

Heteroreceptor in cholinergic neurons

46
Q

What can excessive dopamine cause ?

A

Schizophrenia

  • antipsychotics and neuroleptics treat this disorder because they have a high affinity for dopamine receptors and block the release
  • although their effects are beneficial in the limbic and cerebral cortex they reduce fine motor control in the basal ganglia and cerebellum

Neurobiology (30 decks)

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