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BMS Neuroscience > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

Criteria for neurotransmitters

A
  • Present in the pre-synaptic terminals
  • Released in response to stimulation
  • Able to interact with postsynaptic receptors
  • Rapidly removed from the synapse
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2
Q

What do neurotransmitters need mechanisms for?

A
  • Synthesis and/or storage
  • Release
  • Receptors
  • Transmitter removal
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3
Q

Types of neurotransmitters?

A
  • Acetylcholine
  • Amino acids eg. GABA/glycine
  • Biogenic amines e.g. dopamine/adrenaline
  • Neuropeptides e.g. enkephalin
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4
Q

Characteristics of amino acid and amine NTs

A
  • Small molecules
  • Stored and released from synaptic vesicles
  • Many activate both ligand-gated channel receptors and G-coupled receptors
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5
Q

Characteristics of peptide NTs

A
  • Large molecules
  • Stored in secretory granules
  • Only activate G coupled receptors
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6
Q

What is Dale’s principle?

A

A single neuron has only one neurotransmitter

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7
Q

Why is Dale’s principle violated?

A

Many peptide-containing neurons have both peptide transmitter and an amino acid or amine NT

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8
Q

Which amino acids are abundant in all cells?

A

Glutamate and glycine

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9
Q

Where is synthesis localised to for ACh, GABA and amines?

A

Axon terminal by specific enzymes

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10
Q

What is the most common excitatory transmitter in the CNS?

A

Glutamate

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11
Q

Which receptors does glutamate bind to?

A

AMPA and NDMA

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12
Q

What does glutamate binding to AMPA receptors trigger?

A

Na+ and K+ currents producing an EPSP

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13
Q

How are NMDA receptors activated?

A

Indirectly by another transmitter other than glutamate as they have a voltage-dependent Mg+ block

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14
Q

What is the most common inhibitory transmitter in the brain?

A

GABA

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15
Q

What does too much GABA action cause?

A

A coma

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16
Q

What does too little GABA action cause?

A

Seizures

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17
Q

What channels does GABA use?

A

GABA-gated chloride channels (produces IPSP)

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18
Q

Where is GABA found?

A

Primarily in the brain - especially in the cortex and striatum

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19
Q

What is disinhibition?

A

Inhibiting inhibition

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20
Q

How are peptides synthesised?

A

Formed int he rough ER and packaged into secretory granules

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21
Q

What are the main types of opiate receptors?

A

Mu (µ), kappa (κ) and sigma (σ)

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22
Q

Opiate effect on spinal cord

A

Block pain signal

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23
Q

Opiate effect on periaqueductal grey

A

Regulates sensation of pain

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24
Q

Opiate effect on amygdala

A

Regulates emotional aspect

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25
Q

Opiate effect on frontal cortex

A

Cognitive aspects

26
Q

Opiate effect on brain stem (medulla)

A

Depress respiration and cough reflex (may induce vomiting)

27
Q

What type of receptors are opiate receptors?

A

G-coupled

28
Q

Therapeutic uses of opiates

A

Analgesia - reduces perception of and emotional response to pain
Intestinal disorders - reduces diarrhoea and decreases dehydration
Antitussive - cough suppressant (codeine)

29
Q

Problems with opiates

A
  • Tolerance and dependence develop
  • Analgesic and euphoric effects are linked
  • Analgesic and dependence liability are linked
  • Relieve dull visceral pain better than sharp pain
30
Q

Diffuse modulatory systems of the brain

A
  • Cause effects over large areas of the brain
  • Core nuclei in central part of the brain (often brain stem)
  • Neurons may contact large numbers of postsynaptic neurons
  • ‘Hosepipe effect’
31
Q

Which transmitters are involved in the diffuse modulatory systems?

A
  • Catecholamines (dopamine, noradrenaline, adrenaline)
  • Serotonin
  • ACh
32
Q

Which places is ACh distributed?

A
  • Autonomic nerves
  • Neuromuscular junction
  • Basal forebrain
  • Hippocampus
33
Q

What is ACh associated with?

A
  • Memory
  • Co-ordination
  • Sleep cycle
  • Mood
  • Aggression
34
Q

Which neurotransmitter is lost in Alzheimer’s?

A

ACh

35
Q

What prevents the release of ACh?

A

Botulinum toxin (used in botox)

36
Q

What are some acetylcholinesterase (AChE) inhibitors?

A
  • Nerve gas
  • Insecticides
  • Alzheimer’s treatments
37
Q

What blocks nicotinic ACh receptors?

A
  • Curare

- a-bungarotoxin

38
Q

What blocks muscarinic ACh receptors?

A

Atropine

39
Q

What are catecholamine systems associated with?

A

Movement, mood, attention and visceral function

40
Q

What is L-dopa synthesised from?

A

Tyrosine + Tyrosine hydroxylase (TH)

41
Q

What is dopamine synthesised from?

A

L-dopa + dopa decarboxylase

42
Q

What is noradrenaline synthesised from?

A

Dopamine + dopamine b-hydroxylase (DBH)

43
Q

What is adrenaline synthesised from?

A

Noradrenaline + phentolamine N-methyltransferase (PNMT)

44
Q

How many people over 70 does Parkinson’s affect?

A

1 in 200

45
Q

Symptoms of Parkinson’s

A
  • Tremor
  • Rigidity
  • Akinesia (loss of power of movement)
  • Postural changes - stoop and shuffling gait
  • Monotonus slurred speech
  • No sensory loss
  • Normal cognitive function (at the start)
46
Q

Pathology of Parkinson’s

A

Diminished substantia nigra seen

47
Q

What do striatum do?

A

Inhibit motor function

48
Q

What goes wrong in Parkinson’s disease?

A
  • Dopamine usually inhibits cells of the striatum via D2 receptors (decreases their inhibitory action)
  • This inhibition is lost in Parkinson’s and so inhibition is increased, therefore motor function is inhibited
49
Q

Treatments for Parkinson’s

A
  • L-dopa (increases dopamine)
  • Cocaine blocks re-uptake of DA
  • Selegiline
50
Q

Problems with L-dopa treatment

A
  • Drug becomes ineffective in long term

- Chronic L-dopa syndrome - dopa-induced dyskinesias fluctuating with sudden and severe immobility (on-off syndrome)

51
Q

What is a problem with antipsychotic medication acting on DA receptors?

A

May induce Parkinson’s

52
Q

Where does the noradrenaline system arise from?

A

The locus coeruleus

53
Q

What is the noradrenaline system associated with?

A

Attention, arousal, learning and memory, anxiety

54
Q

How are catecholamines broken down and removed?

A
  • Most reuptake into the presynaptic terminal
  • Metabolised by catechol-O-methyltransferase (COMT) mainly in the cytoplasm
  • Monoamine oxidase (MAO) on outer mitochondrial membrane
55
Q

What does MAO-A metabolise?

A

Mainly NA and 5-HT

56
Q

What does MAO-B metabolise?

A

Mainly dopamine

57
Q

MAO-inhibitors have been used to treat…?

A

Depression - increases NA + 5-HT

Parkinson’s - increases dopamine

58
Q

What is 5-HT also known as?

A

Serotonin

59
Q

Functions of serotonin?

A
  • Consciousness/arousal
  • Circadian rhythms
  • Mood
  • Aggression
60
Q

Treatment of depression

A
  • Tricyclic antidepressants - block serotonin and NA uptake
  • SSRIs - e.g. Prozac
  • MAO-A inhibitors

BMS Neuroscience (23 decks)

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