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Clinical Neuroscience > 2.1.2 Neurotransmitters > Flashcards

2.1.2 Neurotransmitters Flashcards

1
Q

What are the 3 classes of neurotransmitters in the CNS?

A

Amino acids
Biogenic amines
Peptides

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2
Q

What are some examples of each neurotransmitter class?

A

Amino acid
-Glutamate
-GABA
-Glycine

Biogenic amines
-ACh
-NorAd
-Dopamine
-Serotonin (5-HT)
-Histamine

Peptides
-Somatostatin
-Cholecystokinin
-Dynorphin

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3
Q

What are amino acid neurotransmitters responsible for?

A

Excitation and inhibition

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4
Q

What amino acid neuotransmitters are excitatory?

A

Glutamate
Major excitatory neuotransmitter, over 70% of all CNS synapses are glutamatergic

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5
Q

What amino acid neuotransmitters are inhibitory?

A

GABA
Glycine

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6
Q

What are the two types of glutamate receptors?

A

Ionotropic
Metabotropic

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7
Q

What are the 3 different types of ionotropic receptors?

A

AMPA
Kainate
NMDA

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8
Q

What type of receptors are ionotropic receptors?

A

Ion channel- permeable to Na+ and K+, NMDA also permeable to calcium

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9
Q

What does activation of an ionotropic receptor cause?

A

Depolarisation, increased excitability

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10
Q

What receptor is metabotropic?

A

mGluR1-7

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11
Q

What type of receptor is a metabotropic receptor?

A

GPCR

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12
Q

What are metabotropic GPCRs linked to when activated?

A

Changes in IP3 and Ca2+ mobilisation

or

Inhibition of adenylate cyclase and decreased cAMP

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13
Q

What happens to ionotropic receptors with excitatory neurotransmitters?

A

Depolarisation of post-synaptic cell by acting on the ligand-gated ion channels

This leads to excitatory synaptic potenital and depolarisation resulting in more action potentials

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14
Q

What is an excitatory postsynaptic potential?

A

Depolarisation to threshold which makes the cell more likely to fire APs

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15
Q

What receptors do glutamatergic synapses have?

A

AMPA and NMDA

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16
Q

What do AMPA and NMDA receptors do in glutamatergic synapses ?

A

AMPA- mediates the initital fast depolarisation

NMDA- permeable to Ca2+, need glutamate to bind and the cell can be depolarised to allow ion flow through channel
(glycine acts as a coagonist)

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17
Q

What important role do glutamate receptors have?

A

Important in learning and memory

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18
Q

What effect does activation of NMDA and mGluRs have?

A

Up-regulate AMPA receptors

Strong, high frequency stimulation causes long term potentiation (LTP)

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19
Q

What is important for induction of long term potentiation in glutamate receptors?

A

Ca2+ entry through NMDA, strengthens the synapse

Too much Ca2+ causes excitotoxicity, too much gluatamate-excitiotoxicity

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20
Q

What is the main inhibitory transmitter in the brain?

A

GABA

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21
Q

What is the main inhibitory neurotransmitter in the brainsteam and spinal cord?

A

Glycine

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22
Q

How do glycine and GABA lead to inhibitory effects?

A

GABAa and glycine receptors have integral Cl- channels

Opening the Cl- channel causes hyperpolarisation, this brings the cell further from the threshold

Causes inhibitory post-synaptic potential, decreases action potential firing

23
Q

What is the resting membrane potential for cells?

A

~-60mV

24
Q

What is the role of GABAb GPCRs?

A

Modulatory role

25
Q

What two drug types bind to GABAa receptors?

A

Barbiturates and benzodiazepines

Both enhance the response to GABA

26
Q

What do barbiturates do?

A

Axiolytic (reduces anxiety) and sedative actions

No longer used for these reasons as risk of fatal overdose, dependence and tolerance

Sometimes used as anti-epileptics

27
Q

What do benzodiazepines do?

A

Sedative and anxiolytic effects

Used to treat anxiety, insomnia and epilepsy

28
Q

Where is glycine present in high concentration?

A

Spinal cord and brainstem

29
Q

What happens to glycine in the knee jerk reflex?

A

Inhibitory interneurones in spinal cord release glycine to relax the hamstring muscles (antagonist muscles) during knee jerk

30
Q

Apart from glutamate, GABA and glycine what are the role of other transmitters?

A

Modulatory role in the CNS or discrete pathways

31
Q

Where is ACh used as a neurotransmitter?

A

Neuromuscular junction (nicotinic)

Ganglion synapse in ANS (between the pre and post ganglionic neurones)

Postganglionic parasympathetic

CNS

32
Q

How does ACh act in the brain?

A

Acts at both nicotinic and muscarinic receptors in the brain

Mainly excitatory

33
Q

Why are receptors often present on presyanptic terminals?

A

Enhances the release of other neurotransmitters

34
Q

Where do cholinergic neurones originate in the CNS?

A

Basal forebrain (Nucleus basalis)
Brainstem

35
Q

Where do cholinergic pathways from the nucleus basalis go to?

A

Diffuse projections to many parts of cortex and hippocampus

There are also local cholinergic internurones e.g. corpus striatum

36
Q

What are cholinergic pathways involved in?

A

Choline Makes MyCar Awfully Light

Arousal
Learning
Memory
Motor control

37
Q

What is degernation of cholinergic neurones associated with?

A

Degeneration in the nucelus basalis is associated with Alzheimer’s disease

38
Q

What can be used to alleviate symptoms of Alzheimer’s disease?

A

Cholinesterase inhibitors, enhances amount of ACh around (prevents as much breakdown occurring)

39
Q

What are the 3 dopaminergic pathways in the CNS?

A

Nigrostriatal- connects the substantia nigra pars compacta to the dorsal striatum motor control involvement

Mesocortical-midbrain to the cortex
Mesolimbic- midbrain to the amygdala

Both involved in mood, arousal and reward

40
Q

What conditions are associated with dopamine dysfunction?

A

Parkinson’s disease
Schizophrenia
Huntington’s disease

41
Q

What happens in parkinson’s disease?

A

Associated with loss of dopaminergic neurones

Loss of substantia nigra input to corpus striatum

Treat with levodopa- converted to dopamine by DOPA decarboxylase (AADC)

42
Q

What happens in schizophrenia?

A

Release of too much dopamine

Amphetamines release dopamine and NorAd which produces schizophrenic-like behaviour

43
Q

How is schizophrenia treated?

A

Antipsychotic drugs, which are antagonists at dopamine D2 receptors

44
Q

How is carbidopa used in treatment of parkinson’s?

A

Carbidopa is unable to pass the BBB

Levodopa is converted both in the periphery and the brain to dopamine

Levodopa crosses BBB by large neutral amino acid transporters

To ensure more levodopa makes it to the brain to be converted to dopamine, carbidopa is given which inhibits DOPA decarboxylase (AADC)

Levodopa makes it to the brain, carbidopa cannot pass through so levodopa can freely be converted to dopamine by AADC

45
Q

Where does NorAd work as a transmitter?

A

Transmitter at postganglionic (effector syanpse in ANS)

Acts as a neurotransmitter in CNS

46
Q

What does NorAd bind to?

A

G-protein coupled alpha and beta adrenoceptors (same in brain and periphery)

47
Q

Where are the cell bodies of NorAd containing neurones found?

A

Pons and medulla
(mainly from neurones in locus coerules)

48
Q

Where does NorAd release to?

A

Throughout cortex, hypothalamus, amygdala and cerebellum

49
Q

When are NorAd neurones active?

A

Locus coeruleus neurones inactive during sleep

Activity increases during behavioural arousal

Amphetamines increase release of NorAd and dopamine which increases wakefulness

50
Q

NorAd deficiency can be associated with what?

A

Depression, relationship between mood and state of arousal

51
Q

Where do serotonergic pathways in the CNS originate from?

A

Raphe nuclei, extending diffusely to the cerebellum, cortex and the amygdala

Similar distribution to NorAd neurones

52
Q

What is the function of serotonergic pathways?

A

Sleep/wakefulness
Mood

53
Q

What are SSRIs used for?

A

Treat depression and anxiety disorders

Serotonin uptake reduced, more serotonin around increases its effects on receptors

Clinical Neuroscience (45 decks)

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