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A PA20023 > Amine neurotransmitters > Flashcards

Amine neurotransmitters Flashcards

1
Q

What is a monoamine

A
  1. Monoamine- contain one amino acid attached to an amino group
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2
Q

Describe basic of dopamine and noradrenaline structure

A
  1. Derived from tyrosine

2. Contain catechol group

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3
Q

Describe amine systems in the CNS

A
  1. Cell bodies are restricted to a small number of brainstem nuclei
  2. Axons project widely and diffusely throughout the nervous system
  3. Modulate (+ or -) fast excitation or inhibition via multiple receptors
  4. Lack specialised synaptic contacts (cf. glutamate and GABA)
  5. Key roles in arousal, attention, sleep and survival
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4
Q

Describe the diffuse amine modulatory systems

A
  1. Have neurons which have bouton
  2. Where neurotransmitters can be released
  3. Work on receptors that are located extrasynaptically – pre and post
  4. Modulating transmitter release
  5. Can make normal transmission generate an action potential
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5
Q

What are synaptic boutons

A
  1. Synaptic boutons are typically the sites where synapses with other neurons are found, and neurotransmitters are stored here to communicate with other neurons via these synapses.
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6
Q

Describe the noradrenaline pathway in CNS

A
  1. Origin in locus coeruleus- Provides basically all noradrenaline
  2. Diffuse innervation of forebrain, particularly cerebral cortex
  3. Also descending pathways- Modulate pain signals
  4. “Arousal chemical”- Plays key role in attention, vigilance and memory
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7
Q

Describe action of Noradrenaline in CNS

A
  1. Acts at alpha-1, alpha- 2, beta-1 and beta-2 receptors - (GPCR)
  2. Brainstem - blood pressure control - baroreceptor reflex
  3. Descending - movement and pain
  4. Ascending - arousal and mood
  5. Cognitive processes, learning and memory, movement, attention
  6. Depletion in forebrain (cortex, hippocampus) - involved in depression
  7. Overactivity in mania
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8
Q

Describe noradrenaline synthesis

A

1, Identical to autonomic nervous system

  1. substrate is tyrosine
  2. Tyrosine hydroxylase converts tyrosine to L-DOPA
  3. Hydroxylation to L-DOPA - rate limiting
  4. Decarboxylation to dopamine by DOPA decarboxylase
  5. Dopamine taken into vesicles by vesicular monoamine transporter
  6. beta-hydroxylation within vesicles by dopamine-Beta-hydroxylase
  7. Only NA neurones express dopamine-b-hydroxylase
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9
Q

WHat are some important points about synthesis of noradrenaline

A
  1. Tyrosine Hydroxylase and DbetaOH synthesis increased on demand
  2. TH blockade depletes NA - depression
  3. TH saturated - NA unaltered by increased substrate
  4. Synthesis increased by L-DOPA
  5. Blockade of vesicular uptake - reserpine – depression
  6. Depletes nerve terminals of noradrenaline
  7. Use as a model to precipitate depression
  8. N.B. Autonomic side effects
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10
Q

Describe noradrenaline inactivation

A
  1. Reuptake by noradrenaline transporters in nerve terminals- Uptake 1
  2. Degradation by monoamine oxidase (MAO) and catechol-o-methyltransferase (COMT)
  3. Take back up into synapse by transporters where they meet MAO and COMT
  4. Also uptake into glial cells where noradrenaline can be broken down
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11
Q

What are important points about noradrenaline inactivation

A
  1. MAO inhibitors - antidepressant
  2. COMT overexpression - schizophrenic phenotype
  3. Uptake 1 most important
  4. Uptake blockers - antidepressant
  5. Cocaine blockade of uptake - reward- not specific also blocks dopamine uptake
  6. Amphetamine - NA displacement - stimulatory effects
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12
Q

Describe the dopamine pathway in CNS

A
  1. midbrain origin - SN and VTA-
  2. Nigro-striatal pathway
  3. VTA to cortex and hippocampus - mesolimbic/mesocortical pathways
  4. Tubero-infidibular system from hypothalamus to pituitary
  5. “Reward chemical”
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13
Q

What receptors does dopamine act on

A
  1. Acts at D1-5 receptors - all GPCR
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14
Q

What is dopamine involved in

A
  1. Control of movement - nigro-striatal
  2. Control of attention, emotion and reward
    - mesocorticolimbic system
    - Schizophrenia
  3. Involved in action of drugs of abuse (cocaine, heroin, amphetamine)
  4. Control of endocrine function
    - TI system controls pituitary hormone output
    - Why some drugs used to help with schizophrenia can result in endocrine disfunction
  5. Brainstem - vomiting
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15
Q

Describe dopamine synthesis

A
  1. As NA- tyrosine is substrate etc
  2. No DbetaOH in vesicles
  3. Only release DA
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16
Q

Describe dopamine inactivation

A
  1. Inactivation via uptake, MAO and COMT

2. Uptake transporter specific for DA

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17
Q

What diseases is dopamine related to

A
  1. Parkinson’s disease - NS degenerates
  2. L-Dopa, MAO inhibitors and COMT inhibitors - Parkinson’s treatment
  3. Schizophrenia - over-activity in DA mesolimbic/cortical pathways
  4. Psychotropics block DA receptors
    - Parkinson’s-like side effects
    - Hormonal imbalance via TI pathway
18
Q

What does MDMA do

A
  1. MDMA - (3,4-methylenedioxy-N-methamphetamine)
  2. Increases brain 5-HT (and DA and NA)
  3. Increases the hormone oxytocin
  4. “empathogenic”- experience empathy for fellow humans
19
Q

Describe 5-HT pathways in the CNS

A
  1. 5-Hydroxytryptamine (5HT) = serotonin
  2. Arise from raphe nuclei
  3. Forebrain and from dorsal and median raphe
  4. Caudal raphe to cerebellum
  5. Pontine neurones to spinal cord
  6. “Appetites chemical”
20
Q

What are the 5-HT receptors

A
  1. Receptors - 5HT1-7
  2. Sub sets within these receptors
  3. All GPCR except 5HT3 – ion channel
21
Q

What does 5-HT control

A
  1. Control of mood
  2. Control of sleep
  3. Control of feeding
  4. Control of sensory transmission
22
Q

How does 5-HT control mood

A
  1. Cortical/limbic system projections

2. Dysfunction in depression

23
Q

How does 5-HT control sleep

A
  1. Thalamus
  2. Activation - wakefulness/insomnia
  3. Decreased activity - sleep and sedation
24
Q

How does 5-HT control feeding

A
  1. hypothalamus/limbic system
  2. Increase - loss of appetite and weight
  3. Decrease - feeding/weight gain
25
Q

How does 5-HT control sensory transmission

A
  1. Gating of spinal transmission (pain)

2. Cortical inputs dampen sensory overload

26
Q

Describe 5-HT synthesis

A
  1. Substrate dietary tryptophan
  2. Uptake and hydroxylation- via specific amino acid transporter proteins into nerve terminals
  3. tryptophan hydroxylase converts it to 5-hydroxytryptophan
  4. Decarboxylation by AADC To 5-hydroxytryptamine
  5. Concentration into vesicles
27
Q

Describe inactivation of 5-HT

A
  1. inactivation by re-uptake and MAO (5HIAA)

2. Uptake specific for 5HT (not DA/NA)

28
Q

What regulates serotonin availability

A
  1. Tryptophan hydroxylase not saturated
  2. What regulates serotonin availability is availability of tryptophan
  3. Tryptophan is rate limiting
  4. Tryptophan or 5HTP - increase 5HT synthesis – antidepressant?
29
Q

How is 5-HT linked to depression

A
  1. Vesicular uptake blocked by reserpine
  2. 5HT depletion - depression
  3. Inactivation by re-uptake
  4. Blocked by antidepressants - SSRIs
30
Q

What is acetylcholine linked to

A
  1. Acetylcholine - the memory chemical

2. Drugs used to treat Alzheimer’s boost acetylcholine levels

31
Q

Describe acetylcholine pathways in the CNS

A
  1. Projection to cortex/limbic system from magnocellular neurones
  2. Projection to hippocampus- Key part of learning and memory
  3. Projections from brainstem to thalamus and other sites
  4. Local interneurones in basal ganglia
  5. “Memory/motivation chemical”
32
Q

What type of receptors does ACh bind to

A
  1. Both nicotinic (ionotropic) and muscarinic (GPCR)

2. Different to ones present in skeletal muscular junctions

33
Q

What roles does ACh play

A
  1. Arousal, sleep, waking
    - Reticular activating system from brainstem
    - Increased ACh - arousal (and vice versa)
  2. Basal forebrain nuclei involved in cognition
    - Degeneration in Alzheimer’s disease
  3. Learning and memory
    - Septo-hippocampal pathway
    - Alzheimer’s disease
34
Q

Describe ACh synthesis

A
  1. Same as NMJ
  2. Substrate dietary choline
  3. Active uptake
  4. If meets acetyl Coenzyme A then choline acetyltransferase converts it to acetyl choline
  5. Acetyl CoA from mitochondria- Acetylation of choline (ChAT)
  6. Active transport into vesicles
35
Q

What is rate limiting in ACh synthesis

A
  1. ChAT not saturated - choline rate limiting

2. Choline increases ACh synthesis

36
Q

Describe inactivation ACh

A
  1. Inactivation by acetylcholinesterase in synaptic cleft
  2. Free choline + acetic acid
  3. Active uptake of choline
  4. Increasing ACh - Alzheimer’s therapy
37
Q

What is histamine produced from

A
  1. Histamine produced from the amino acid histidine
  2. Storage, release and reuptake mechanisms not well defined
    6)
38
Q

Where is histamine synthesised and localised

A
  1. Synthesized and localized to the tuberomammillary nucleus within the hypothalamus
39
Q

What are the histamine receptors

A
  1. Histamine H1, H2, H3 and H4 receptors are GPCRs

2. Histamine neurons project to monoamine and cholinergic neurons involved in arousal, attention, learning and memory.

40
Q

What roles to histamine play

A
  1. Histamine plays a role in sleep

2. Histamine plays a role in feeding and energy balance

41
Q

What drugs used to target Histamine receptors

A
  1. Diphenhydramine (Benadryl) is a CNS penetrant H1 antagonist that is sedating (also muscarinic AChR antagonist)
  2. Newer allergy antihistamines (e.g. loratadine) don’t cross the BBB
  3. Histamine H2 antagonists (e.g. cimetidine) don’t cross the BBB

A PA20023 (19 decks)

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