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Physiology 2 > Monoamines > Flashcards

Monoamines Flashcards

1
Q

What does the autonomic nervous system control?

A

• Autonomic nervous system – controls behaviour (not under voluntary control.)

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2
Q

What does the sympathetic nervous system control?

A

• The sympathetic nervous system is for body activation e.g fight of flight response

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3
Q

What does the parasympathetic nervous system control?

A

• The parasympathetic nervous system is for relaxation, recovery. S/P and opposite effects, when one turns off the other turns on

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4
Q

What system are the monoamines part of?

A

The monoamine system forms part of the Diffuse Modulatory Systems (neurones that release monoamines e.g adrenaline, dopamine neurons) of the brain

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5
Q

What are the common principles of the monoamine system?

A
  • 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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6
Q

What are the 4 main systems?

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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7
Q

What are the Diffuse Modulatory Systems of the Brain (synapses)?

A

A: Point to point communication e.g GABA and glutamate as learned in previous lecture
-Fast, restricted
B: Diffuse modulatory systems e.g dopamine (they modulate an excitation or inhibit)
-slower, widespread

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8
Q

Where is noradrenaline released from?

A

Noradrenaline is released from noradrenergic neurones.

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9
Q

What do the cell bodies of noradrenaline neurones give rise to?

A

• Cell bodies for NAergic neurons – main one in LC – gives rise to millions of NAergic nerve terminals throughout the cortex, hippocampus and cerebellum. Release transmitter diffusely (i.e. like an aerosol)

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10
Q

What is the function of the hypothalamus, Thalamus, locus coeruleus and Temporal lobe?

A
  • Hypothalamus – hormones, sleep, body temperature, endocrine and autonomic controller)
  • Thalamus – main relay station for most information going into the brain
  • Locus coeruleus –known as ‘blue spot’ because of pigmentation. NA in this region makes brain more responsive, increases information processing – LC involved in attention, arousal, anxiety, sleep/wake. Neurons most active when novel stimuli presented (when animal is vigilant). Low arousal associated with low NA e.g. depressed patients.
  • Temporal lobe = deep within the temporal lobe = amygdala
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11
Q

What are the 5 functions of noradrenaline?

A
  • Arousal
  • Wakefullness
  • Exploration and mood (low NA in depressed)
  • Blood pressure
  • Addiction/gambling
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12
Q

How is noradrenaline synthesised?

A
  • We start of with tyrosine which is converted to DOPA by tyrosine hydroxylase
  • DOPA is metabolised to Dopamine by DOPA decarboxylase
  • Dopamine is then hydrolysed to noradrenaline by Dopamine beta hydroxylase
  • Noradrenaline can then by converted to adrenaline
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13
Q

How is NA regulated?

A 
•	Post-synaptic
	Carry on the message
•	Pre-synaptic (autoreceptors)
	Usually inhibitory
	Negative feedback  mechanism

On image

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14
Q

What are the receptor noradrenaline binds to?

A

On image

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15
Q

What drugs regulate noradrenaline?

A

Reserpine
• Prevent storage of NA in vesicles – NA in cytosol broken down by MAO
• Reduces NA release
• Less sympathetic actions, e.g. Less 1-mediated vasoconstriction
• Early treatment for hypertension
• Set principle for future treatments – reduce sympathetic nerves reduce BP

Amphetamine / Ephedrine
• Reverses uptake transporters causing release of NA into cleft
• Ephedrine (decongestant) – vasoconstriction of nasal blood vessels

Guanethidine
• Compete with NA for inclusion into vesicles, reduces NA release

Clonidine / -methyl-DOPA
• Stimulate pre-synaptic 2 receptors, reduces NA release
Cocaine-blocks NA re-uptake

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16
Q

Where is dopamine released from?

A

• Dopamine is released from dopaminergic neurones
• One branch of dopaminergic neurones project from the Substantia nigra which release them at the striatum where dopamine is released causing movement. Parkinson’s disease therefore affects movement
• Dopaminergic neurones also have a core at the VTA and project to the nucleus accumbens needed for reward and pleasure and to the amygdala for emotionality and the hippocampus needed for memory and learning
• Mesocortical pathway releases dopamine to the frontal cortex of the brain
• Tuberohyphyseal pathway – prolactin secretion.
o Dopamine is also produced in the hypothomes and is transported via the portal system to the pituitary glands where it activates dopamine D2 receptor that inhbits prolactin
• Dopamine receptors are also found in the chemoreceptive trigger zone, activation of this causes vomiting

17
Q

What are the functions of dopamine?

A

On image

18
Q

How is Dopamine synthesised?

A
  • We start of with tyrosine which is converted to DOPA by tyrosine hydroxylase
  • DOPA is metabolised to Dopamine by DOPA decarboxylase
  • Dopamine is then hydrolysed to noradrenaline by Dopamine beta hydroxylase
  • Noradrenaline can then by converted to adrenaline
19
Q

How is Dopamine regulated?

A
  • Once Dopamine is produced it enters vesicles for storage until it is released into the synaptic cleft.
  • Dopamine will then activate Dopamine D1 and D2 (negative feedback – inhibits dopamine release) receptors
  • There are also dopamine transporters on the pre-synaptic neurones that can reuptake dopamine when there is too much. It is then broken down by monoamine oxidase B
20
Q

How can we increase levels of Dopamine?

A
  • Administer L-dopa
  • Block dopamine transporters so it cannot be reuptake into the pre-synaptic neurone
  • Inhibit monoamine oxidase B – so dopamine increases and leaks out
  • Selegiline drug – it blocks monoamine oxidase B
21
Q

What receptors does dopamine act upon?

A

On image

22
Q

Describe the distribution of serotonin (5-HT) receptors

A

• Distribution of 5-HT neurons resembles that of NA. Cell bodies grouped around the midline (ridge/ raphe). 9 raphe nuclei and each nucleus projects to different regions of the brain (cortex, striatum, thalamus (rely of all information), hypothalamus (heat regulation), hippocampus and amygdala, cerebellum and spinal cord (pain modulation).

23
Q

What does serotonin cause?

A

On image

24
Q

How is serotonin synthesised?

A
  • Tryptophan is the precursor and is metabolised to 5-hyroxytryptophan by Tryptophan hydroxylase
  • 5-hyroxytryptophan is then metabolised to 5-hyrdoxytryptamine (serotonin) via dopa decarboxylase
  • 5-hyrdoxytryptamine (serotonin) is further metabolised 5-hydroxyindoleacetylaldehyde by monoamine oxidase
25
Q

Where is serotonin stored?

What receptors does it act upon?

What is 5HT1D?

What uptakes serotonin?

What causes depression?

A
  • Serotonin is transported into serotonin vesicles for storage
  • It is then released into the synaptic cleft where it will bind to Serotonin receptors (15 subtypes, all GPCR except 5HT which is an ion channel)
  • 5HT1D is an auto receptor, found on the pre-synapse. This inhibits serotonin release.
  • High levels of serotonin is reduced by serotonin transporters on the pre-synaptic cleft which is then broken down monoamine oxidase
  • Depression is caused by a deficit of 5-HT, so a drug that increases it can reverse the symptoms of this. We can do this by blocking the serotonin transporters so it cannot be uptaken back into the pre-synaptic neurone. You can also inhibit monoamine oxidase so it accumulates and leaks out into the synaptic cleft
26
Q

What are the cell bodies and terminals of 5-HT, dopamine and noradrenaline

A

On image

27
Q

What are the transporters?

A

On image

28
Q

Where is acetylcholine released from?

A
  • Cholinergic neurones release acetylcholine
  • Some originate in the nucleus basalis and project to the cortex
  • Other cholinergic neurones can project from the septum to the hippocampus
  • Other cholinergic neurones can project from the substantia nigra to the thalamus
  • There are also neurones in the striatum.
  • They act on nicotinic receptors (ion channels) and muscarinic receptors (GPCR)
29
Q

What is acetylcholine involved in?

A
  • Memory, learning
  • Motor control (striatum)
  • Reward
  • Arousal
30
Q

How is acetylcholine synthesised?

A

On image

31
Q

What receptors does acetylcholine bind to?

A
  • M1 excitatory ( M1 receptors in dementia)
  • M2 presynaptic inhibition (inhibit Ach release)
  • M3 excitatory glandular/smooth muscle effects (side effects)
  • M4 and M5 function not well known
32
Q

What are the functions of histamines, purines and neuropeptides?

A

Histamine
• H1 (arousal) and H3 (presynaptic / constitutively active)
• Functions: sleep / wake, vomiting
Purines
• Adenosine (A1, A2A/2B) and ATP (P2X)
• Functions: sleep, pain, neuroprotection, addiction, seizures, ischaemia, anticonvulsant
Neuropeptides
• Opioid peptides
o , , 
• Tachykinins (Substance P, neurokinin A & neurokinin B)
o NK1 (Substance P), NK2 (neurokinin A), NK3 (neurokinin B)
• Functions: pain

33
Q

Have a look at the Opioid peptides and opioid receptors

A

On image

34
Q

What do lipid mediators and melatonin cause?

A

Lipid mediators
• -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)
Melatonin
• -MT1, MT2 receptors
• involved in sleep regulation, circadian rhythmicity, agonists for jet lag and insomnia

35
Q

What does Amphetamine do and what are the pharmacological effects?

A

• Amphetamine-like drugs (methylphenidate & MDMA)
• Release cytosolic monoamines (DA)
• Prolonged use neurotoxic
 Degeneration of amine-containing nerve terminals, cell death
Pharmacological effects:
• alertness and locomotor stimulation ( aggression)
• Euphoria / excitement
• Stereotyped behaviour
• Anorexia
• physical and mental fatigue (improves monotonous tasks)
• Peripheral sympathomimetic actions ( blood pressure &  gastric motility)
• Confidence improves/lack of tiredness
Therapeutic uses
• ADHD (methylphenidate), appetite suppressants, narcolepsy

36
Q

What does cocaine do?

What are the pharmacokinects?

A 
•	Blocks catecholamine reuptake 
•	( DA, stimulant effect)
•	Pharmacological effects:
o	Euphoria
o	Locomotor stimulation
	Fewer stereotyped behaviours than amphetamine
o	Heightened pleasure
	Lower tendency for delusions, hallucinations and paranoia

Pharmacokinetics:
• HCl salt, inhaled and i.v. administration
• Nasal inhalation less intense, leads to necrosis of nasal mucosa
• Freebase form (‘crack’), smoked, as intense as i.v route

37
Q

What does MDMA (ecstasy) cause?

A

• Inhibits monoamine transporters (mainly 5-HT)
• Large  5-HT (followed by depletion)
 5-HT linked to psychotomimetic effects
 DA linked to euphoria (followed by rebound dysphoria)

38
Q

What does LSD, Psylocybin?

A

• Hallucinogenic effect by acting on 5HT2 receptors

39
Q

What do Psychostimulants do?

A
  • Also increase 5HT and NA

* Cocaine block DAT, NET, SERT

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