Amine Neurotransmitters Flashcards by Isabel Adcock

Amine Neurotransmitters

Noradrenaline
Dopamine
5-hydroxytryptamine
Acetylcholine

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Key roles of amine neurotransmitters

Roles in arousal, attention, sleep and survival

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Speed of amine system modulation

Can modulate fast excitation or inhibition.
Via multiple receptors

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Location of amine systems

Cell bodies restricted to a small number of brainstem nuclei
Gathered together in clusters, based on which NT they produce
Axons project widely and diffusely throughout the nervous system

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Unlike glutamate and GABA, amine NTs lack…

Specialised synaptic contacts

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Noradrenaline pathways in the CNS

Origin in the brainstem (locus coeruleus)
Diffuse innervation of forebrain, particularly the cerebral cortex
Also descending pathways

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Where does noradrenaline bind

α1, α2, β1 and β receptors – GPCRs
Not at ligand gated ion channels

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Role of noradrenaline in the brainstem

Blood pressure control
Baroreceptor reflex

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Noradrenaline in descending pathways

Movement and pain

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Noradrenaline in Ascending pathways

Arousal and mood
Cognitive processes, learning and memory, movement, attention

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Noradrenaline synthesis

Tyrosine to L-DOPA by tyrosine hydroxylase
Decarboxylated to dopamine by dopamine dopadecarboxylase.
Taken into vesicles by vesicular monoamine transporter
Dopamine-b-hydroxylase converts it

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Modulation of Noradrenaline synthesis

Hydroxylation of tyrosine to L-DOPA is rate limiting.
TH and DβOH synthesis can in increased on demand

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Noradrenaline inactivation

Reuptake by NA transporters into presynaptic terminals
Degradation here by monoamine oxidase (MAO) and catechol-o-methyltransferase (COMT)

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Modulation of Noradrenaline inactivation

Uptake 1 is the most important transporter and can be blocked
Cocaine blocks uptake
Amphetamine makes reuptake transporters release NA

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Dopamine pathways in the CNS have … origin

Midbrain

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Dopamine pathways

Nigro-striatal
Mesolimbic/mesocortical
Tuber-infidibular

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Mesolimbic/mesocortical pathways

VTA to cortex to hippocampus
(Ventral Tegmental Area)

Tuber-infidibular system

From hypothalamus to pituitary

Where does Dopamine act in the CNS

At D1-5 receptors
All GCPRs

Effects of dopamine

Control of movement (nigro-striatal)
Control of attention, emotion and reward
Control of endocrine function
Brainstem - vomiting

Synthesis of dopamine

Tyrosine to L-DOPA by tyrosine hydroxylase
Decarboxylated to dopamine by dopamine dopadecarboxylase.
Taken into vesicles by vesicular monoamine transporter

Inactivation of dopamine

Reuptake by DA transporters into presynaptic terminals
Degradation here by monoamine oxidase (MAO) and catechol-o-methyltransferase (COMT)

Schizophrenia is caused by …

An overactivity on DA mesolimbic/cortical pathways

5HT pathways

Arise from raphe nuclei
Forebrain and from dorsal and median raphe
Caudal raphe to cerebellum
Pontine neurones to spinal cord

5HT receptors

5HT 1-7

Areas of 5HT action

Cortical/limbic system Thalamus Hypothalamus/limbic system Gating of spinal transmission

5HT in the cortical/limbic system

Control of mood Dysfunction in depression

5HT in the thalamus

Control of sleep Activation = wakefulness/insomnia Decreased activity = sleep and sedation

5HT in the hypothalamus/limbic system

Control of feeding Increase = loss of appetite Decrease = feeding/weight gain

5HT in spinal transmission

Control of sensory transmission Gating of spinal transmission (pain) Cortical inputs dampen sensory overload

5HT synthesis

Tryptophan is taken up and hydroxylated Decarboxylation by AADC Concentration into vesicles

Modulation of 5HT synthesis

Tryptophan hydroxylase is not saturated, therefore consuming more tryptophan can cause greater production. Vesicular uptake can be blocked by reserpine

Reuptake of 5HT

Inactivation and reuptake by MAO Uptake is specific for 5HT and can be blocked by SSRIs

Acetylcholine pathways in the CNS

Projection to cortex/limbic system from magnocellular neurons Projection to hippocampus Projections from brainstem to thalamus and other sites Local interneurons in basal ganglia

Receptors for Ach

Both nicotinic (ionotropic) and muscarinic (GPCR)

Ach in the brainstem

Reticular activating system Arousal, sleep and waking Increased Ach = arousal

Ach in the basal forebrain nuclei

Cognition

Ach in the septo-hippocampal pathway

Learning and memory

Ach synthesis

Same as NMJ Choline is taken up (active uptake) Acetyl CoA is added by ChAT Active transport into vesicles

Modulation of Ach synthesis

ChAT is not saturated, so dietary choline is rate limiting

Inactivation of Ach

Inactivation by acetylcholinesterase in the synaptic cleft, into free choline + acetic acid. Active uptake of choline