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Monoamines Flashcards

1
Q

what are the 3 CNS systems that control behaviour?

A

Autonomic nervous system
Hypothalamic-pituitary neurohormones
Diffuse monoamine system

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2
Q

what is the diffuse monoamine system?

A

Four systems, which have common principles:

  • Small set of neurons at core
  • Arise from brain stem
  • One neuron influences many others
  • Synapses release transmitter molecules into extracellular fluid
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3
Q

name the 4 systems that make up the diffuse monoamine system:

A
  • Noradrenergic Locus Coeruleus
  • Serotonergic Raphe Nuclei
  • Dopaminergic Substantia Nigra and Ventral tegmental Area
  • Cholinergic Basal Forebrain and Brain Stem Complexes
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4
Q

name the 4 neurotransmitters that make up the diffuse monoamine system:

A

NA, released from noradrenergic neurons
Serotonin, released from serotonergic neurons
Dopamine, released from dopaminergic neurons
Ach, released from cholinergic neurons

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5
Q

where do the neurotransmitters project from and where do they project to?

A

the 4 neurotransmitters project from the central core (where the cell bodies are) to different brain regions

eg. noradrenergic neurons project from the central core, the Locus Coeruleus - this projects to the cortex, hypothalamus, spinal cord, where noradrenaline is released

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6
Q

what is neurotransmission in the brain like?

A
  1. Fast point-to-point signalling
    Neurotransmitters producing excitatory or inhibitory potentials
    Ligand-gated ion channels
    Glutamate, GABA, ACh
  2. Slow transmission
    Neurotransmitters and neuromodulators
    G-protein coupled receptors
    Monoamines, peptides, ACh
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7
Q

where do neurotransmitters act?

A

when the neurotransmitters are released, they act on receptors
eg. dopamine will act on D1 and D2 receptors

All of these receptors are g-protein coupled receptors – some inhibit AC, some stimulate AC (Gi/Gs coupled), some are Gq coupled, stimulating Phospholipase C

They are NOT ion channels. Given they are not ion channel receptors, transmission is slow.
-dopamine, serotonin, NA

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8
Q

Noradrenergic monoamine system

A

noradrenergic monoamine system

  • consists of noradrenergic neurons (neurons which release NA)
  • they project from the Locus coeruleus to the cortex, amygdala, hypothalamus and cerebellum – NA released in these places
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9
Q

NA post synaptic and pre synaptic receptors

A

NA in vesicles and released into synapse, binds to:

Post-synaptic receptors
-carry on the message

Pre-synaptic receptors

  • autoreceptors
  • inhibit NA release, negative feedback mechanism
  • alpha-2
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10
Q

autoreceptors of the monoamine diffuse system

A

5-HT1A
D2/D3
alpha-2

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11
Q

names of reuptake transporters of the monoamine diffuse system

A

EAAT - glutamate
DAT - dopamine
SERT - serotonin
NET - noradrenaline

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12
Q

structure of reuptake transporters of the monoamine diffuse system

A

12 TMDs (TMD pore in neurone membrane)
Both ends intracellular
Pump monamines in neuron
DA, NA, 5HT transporters

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13
Q

actions of Reserpine and

Cocaine on noradrenaline release

A

Reserpine - depletes NA stores by inhibiting vesicular uptake

Cocaine - blocks NA re-uptake

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14
Q

different actions of adrenoceptors

A

Alpha 1 = Gq coupled, Phospholipase C, SM contraction

Alpha 2 = Gi coupled. These are autoreceptors. Decreased AC

Beta = Gi coupled AC, cAMP, contraction of cardiac muscle, SM relaxation

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15
Q

name an alpha 2 agonist

A

clonidine

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16
Q

actions of NA?

A
  • NAergic neurons active when ‘awake’
  • Arousal, wakefullness, mood (low NA in depressed patients)
  • Blood pressure regulation - play role in reward system
  • Addiction/gambling
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17
Q

too much NA

too little NA

A

: hyper arousal, high BP (cardiovascular problems), gambling problems
too low: depression-like behaviour (opposite of excitement)

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18
Q

actions of amphetamine on noradrenaline release and effects in the body?

A

amphetamine enters vesicles displacing NA into cytoplasm, increase NA leakage out of neurone
- increases alertness and exploratory behaviour

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19
Q

when is there an NA surge?

A

big impulsive-like excitement before you start gambling

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20
Q

Dopaminergic monoamine system

A

Dopamine is released from dopaminergic neurones
4 main pathways
1. Nigrostriatal pathway
-neurons project from the Nigro to the Striatum, where dopamine gets released and acts on dopamine receptors to induce movement (Parkinson’s)

  1. Mesolimbic pathway
    - neurons which project from VTA to amygdala (emotions), hippocampus (learning and memory) and nucleus ocumbus (important region involved in pleasure/reward). This pathway has important role in rewards eg. foods, sex, pleasurable behaviours – the rewards activate the mesolimbic system and induce release of dopamine (schizophrenia)
  2. Mesocortical pathway
    - neurons project from the VTA region to the cortex
  3. Tubero-hypophyseal pathway
    - dopamine released from neurons to activate neighbouring neurons, but can also act as a neurohormone
    - dopamine can be released from the hypothalamus directly to the blood circulation (portal system). Dopamine will go from the hypothalamus to the pituitary, and inhibit the release of prolactin
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21
Q

what do people develop Parkinson-like symptoms?

A

Nigrostriatal neurons degenerate - 80-90% of them start dying, so dopamine levels in the striatum decrease, and as a result you can suppressed/slow movement, and eventually you stop moving

22
Q

drugs of abuse hijack which monoamine system?

A

dopaminergic mesolimbic pathway

  • drugs of abuse hijack this, stimulating the rewards even more, releasing even more dopamine and increasing pleasure.
  • many studies imply that psychotic like behaviour (symptoms of schizophrenia – hallucinations, psychotic episodes) is due to a big hyperactivity of the mesolimbic pathway, leading to a big increase in dopamine release.
23
Q

dopamine and vomiting

A

Dopaminergic system and D2 receptors are important in vomiting – hyper activation of receptors in regions of the brain involved in vomiting eg. chemoreceptor trigger zone induces emesis.
-This is why dopaminergic drugs such as eldopa (great for treating some of the symptoms of Parkinson’s Disease) induces emesis as a side effect as it activates those dopamine receptors in the chemoreceptor trigger zone.

24
Q

Where does dopamine come from?

A

precursor molecule for dopamine is tyrosine

Tyrosine gets metabolised by tyrosine hydroxylase to form DOPA

DOPA gets metabolised by DOPA decarboxylase to form dopamine

tyrosine —— (tyrosine hydroxylase) ——-> DOPA —— (DOPA decarboxylase)—–> DOPA

25
Q

what receptors does Dopamine bind to and what happens when you bind to them?

A

7-TM domain, GPCR
N-terminus found extracellularly, C-terminus found intracellularly

dopamine post-synaptic receptors, D1 and D2
(D1 gap is D1 and D5, D2 grp is D2, 3, 4)
D2 also found pre-synaptically, autoreceptors, inhibit further dopamine release

D1 receptors = Gs coupled, dopamine binding activates AC, increasing cAMP and PKA. PKA phosphorylates and activates DARPP-32, inducing various secondary messenger systems and excitability

D2 receptors are Gi coupled, so they inhibit AC, leading to decreased cAMP levels.

D1 and D2 receptors very often come together and from heterodimers - these are usually Gq coupled, which will lead to activation of phospholipase c and increased IP3, DAG, etc

26
Q

why is it important to regulate the amount of dopamine in the synaptic space, and what happen when we have:

a) too much dopamine
b) too little dopamine

A

too much dopamine = schizophrenia, addiction, psychotic-like symptoms

too low levels of dopamine = parkinson’s-like symptoms, too little movement

therefore, its important to modulate the amount of dopamine in the synaptic space.

27
Q

dopamine reuptake and degradation

A

Dopamine levels are modulated via a reuptake system – dopamine transporters (DAT’s) pump dopamine back into the neuron, where dopamine gets metabolised by monoamine oxidase B

28
Q

how can drugs act to treat the symptoms of Parkinsons? and give an example of a drug

A

these drugs act to increase dopamine levels

  1. block reuptake system - dopamine but can’t get back into the neuron so it accumulates
  2. drug that blocks monoamine oxidase B (selgulin does this)

Eldopa treats symptoms of Parkinsons

29
Q

location of dopamine receptors in the brain

A

D1 and D2 receptors in striatum, limbic system, thalamus & hypothalamus

D3 receptors in limbic system NOT striatum

D4 receptors in cortex & limbic system

30
Q

functions of dopamine

A

Movement, addiction, hormone release, vomiting

31
Q

where is serotonin released from and where does it project to?

A

released from serotonergic neurons which project from the raphe nucleus (where the cell bodies are found), to cortex, cerebellum, striatum, hypothalamus, amygdala, hippocampus, where 5-HT is released and acts on 5-HT receptors

32
Q

what effect will increasing serotonin in the mentioned brain regions have?

A

increase serotonin cortex = heightened perceptions

increase serotonin in hypothalamus = reduced appetite

increase serotonin amygdala = elevate mood

33
Q

how does ecstasy affect serotonin levels?

A

increases serotonin levels

34
Q

what is the precursor for serotonin?

A

5-HT comes from tryptophan
-tryptophan comes from food, because its an essential amino acid – we have to ingest it, our body doesn’t make it naturally

35
Q

too much serotonin = ?

too little serotonin = ?

A

too much serotonin = psychotic-like effects, e.g. hallucinations
too little serotonin = depression

36
Q

serotonin in the synaptic bouton: receptor binding and reuptake

A

serotonin in vesicles, released in the synaptic space and acts on post-synaptic serotonin receptors

  • post synaptic receptors, many diff ones
  • pre-synaptic auto receptors, 5-HT 1D (serotonin binding inhibits serotonin release)

modulates serotonin levels via re-uptake system: serotonin pumped into neuron via serotonin transporters, then metabolised by monoamine oxidases

37
Q

are all serotonin receptors GPCR’s?

A

all but 1

5-HT3 is a LGIC

38
Q

serotonin functions

A
  • Mood (anxiety/depression)
  • Psychosis (5HT antagonism antipsychotic)
  • Sleep / wake (5-HT linked to sleep, 5-HT2 antagonists inhibit REM sleep)
  • Feeding behaviour (5HT2A antagonist increase appetite, weight gain; antidepressants decrease appetite
  • Pain, migraine (5-HT inhibits pain pathway, synergistic with opioids)
  • Vomiting
39
Q

where is acetylcholine released from and where does it project to?

A

3 main pathways

1) Project from the nucleus basalis (where the cell body is found) to the cortex (where Ach is released)
2) project from the septum to the hippocampus
3) project from the substantia nigra to the hypothalamus.

40
Q

degeneration of cholinergic neurones can cause what?

A

neurodegenerative conditions like Alzheimer’s/dementia, causing cognitive impairment (affects memory and learning)

41
Q

how is Ach formed?

A

Choline and Acetyl CoA come together to form Acetylcholine

42
Q

Ach in the synaptic space and receptor binding

A

Acetylcholine will get inside the cholinergic vesicles and released into the synaptic space, where it acts on post-synaptic acetylcholine receptors

2 types of acetylcholine receptors: muscarinic (GPCR’s) and nicotonic (ion channels
muscarinic:
-M1 excitatory - less M1 receptors in dementia
-M2 presynaptic inhibition (inhibit Ach release)
-M3 smooth muscle effects
M4 and M5 function not well known

43
Q

How are Ach levels regulated?

A

Acteylcholinesterase – an eznyme which breaks down Ach to Acetate and Choline, which goes back inside the neuron and gets recycled.

44
Q

what are Ach receptors abundant?

A

basal forebrain, hippocampus and striatum

45
Q

functions of Ach?

A
  • Arousal
  • Epilepsy (mutations of nAChR genes)
  • Learning and memory
  • Motor control, pain, addiction
  • Involved in schizophrenia, ADHD, depression, anxiety, Alzheimers

extremely important for memory and learning, but also involved in addiction, arousal, movement

46
Q

Relationship between Alzheimers and Ach?

A

Alzheimer’s disease associated with loss of cholinergic neurons and memory loss – no real effective treatment.

47
Q

Histamine

A

H1 - arousal, antihistamines cause sedation
H3 - presynaptic, reduce histamine release

Functions: sleep / wake, vomiting

48
Q

Purines

A

Adenosine and ATP
-adenosine is a breakdown product of ATP and acts on adenosine receptors in the brain, involved in sleep and addiction

Functions: sleep, pain, neuroprotection, addiction, seizures, ischaemia, anticonvulsant

49
Q

Neuropeptides

A

Neuropeptides are peptides released from the neurones, act on receptors

  • Opioid peptides (mu, delta and kappa)
  • four opioid receptor types all over the brain
  • Tachykinins

Functions: pain

50
Q

Lipid mediators

A
  • Products of conversion of eicosanoids to endocanabinoids
    • act on CB1 (inhibit GABA, glutamate release)
    • involved in vomiting (CB1 agonist block it, -MS, pain, anxiety, weight loss/rimonabant CB1 antogonist)
51
Q

Melatonin

A
  • MT1, MT2 receptors

- involved in sleep regulation, circadian rhythmicity, agonists for jet lag and insomnia

52
Q

Amphetamine

A

Pharmacological effects:

  • Alertness and locomotor stimulation ( aggression)
  • Euphoria / excitement
  • Stereotyped behaviour
  • Anorexia, physical and mental fatigue (improves monotonous tasks)
  • Increased BP and decreased gastric motility
  • Confidence improves/lack of tiredness

Therapeutic uses
-ADHD (methylphenidate), appetite suppressants, narcolepsy

Neuro (21 decks)

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