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Ageing Flashcards

1
Q

What is the pneumonic of remembering neurotransmission?

What do the stand for

A

X2 S’s = synthesis, storage
X3 R’s = release, receptors, reuptake
X2 D’s = depredation, drugs and disease

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2
Q

What is the main CNS excitatory NT?

A

Glutamate

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3
Q

What is the main CNS inhibitory NT?

A

GABA

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4
Q

What are the 2 types of post-synaptic receptor?

Which works faster?

A

Inotropic = ion channel pore = work faster

Metabotropic = GPCR second messenger system = takes longer

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5
Q

Is there music glutamate in the PNS?

A

No

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6
Q

Where are NT’s synthesised?

A

In the brain

Body takes in precursors

NT”s made in presynaptic neurones where it is needed

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7
Q

Name the 2 pathways in which glutamate is synthesised.

Name the enzymes at each stage if you can.

Include which each pathway happens in.

A

Neuron pathways (in neurons) = glutamine —> glutamate (glutaminase enzyme) —> alpha-oxogluterate (transaminase enzyme)

Glial pathway (glial cell) = alpha-oxogluterate —> glutamate (GABA transaminase enzyme) —> glutamine (glutamine synthase enzyme)

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8
Q

Where is glutamate stored?

How does it get to where it needs to be stored, explain the mechanism.

A

Vesicles in pre-synaptic membrane

vGluT1, 2 and 3 transporter pump puts glutamate in vesicle via hydrogen ion anti-transporter

Hydrogen ion pump (proton pump) pumps H ions into the vesicles to make it acidic then H/glutamate antiporter used to swap H for glutamate

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9
Q

What is the name of the process of glutamate release and what molecules are involved?

A

Calcium dependant vesicular release

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10
Q

Name 3 ionotropic glutamate receptors and the ions they allow to enter or exit once activated.

A

NMDA (Na, K and Ca)

AMPA (Na, K and some Ca)

Kainate (Na and K only)

NB: K is moving out of cells as others move in

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11
Q

Name 3 metabotropic glutamate receptors and the GPCR G-proteins they couple to.

A

Group 1 = mGluR1 and 5 coupled to Gq and G11

Group 2 = mGluR2 and 3 coupled to Go and Gi

Group 3 = mGluR4 and 6-8 coupled to Go and Gi

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12
Q

Where are most NT’s degraded?

Which cells tend to degrade NT’s?

A

Inside the cells

Neurones

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13
Q

Where is Ach degraded?

A

Outside the cell in the post-synaptic cleft by acetlycholinesterase

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14
Q

Which transporter is at play for the reuptake of glutamate?

A

EAAT (excitatory amino acid transporter)d

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15
Q

Which cells reuptake glutamate?

What does each cell do with the glutamate when it has reuptaken it?

A

Neurons = repackaged into vesicles

Astrocytes = synthesised into glutamine by glutamine synthase, then secreted via glutamine transporter, uptakes by neurones via glutamine transporter and finally synthesised back into glutamate and packed into vesicles ready for use

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16
Q

Name a drug which blocks NMDA glutamate receptor ion channels?

What effect does this have?

A

Ketamine

Sedative, analgesic, amnesic

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17
Q

Name a competitive antagonist for the NMDA glutamate ion channel.

What is it used for.

A

Memantine = Alzheimer’s drug

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18
Q

Differentiate between competitive and non-competitive antagonist drugs.

A

Competitive = compete at binding site to block agonist binding site

Non-competitive = bind to an allosteric site (non-agonist binding site) and trigger a conformational change in structure to prevent agonist from binding at site

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19
Q

What is perampenal used for and how does it work?

A

Anti-epileptic drug

Non-competitive antagonist of AMPA receptors (glutamate ion channel)

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20
Q

How does PCP (phencyclidine = street drug) work?

A

NMDA receptor (glutamate ion channel) antagonist

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21
Q

Is there much GABA in the PNS?

A

Very little

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22
Q

What is the precursor GABA molecule?

What enzyme is involved in the reaction?

A

Glutamate!

GAD = glutamic acid decarboxylase

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23
Q

Explain the storage of GABA.

A

Same mechanism as glutamate

VGABAT = transporter responsible

Still uses proton pump and H gradient to move GABA into vesicles

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24
Q

Explaim GABA release.

A

Same as glutamate

Calcium dependant vesicular release

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25
Q

Name the GABA ionotropic receptors.

What anions does this allow to pass?

How does this achieve GABA’s function?

A

GABAa receptor

Chlorine anion channel

Chlorine ions are negatively charged therefore hyperpolarise cell and make it less likely to fire (therefore is an inhibitory NT)

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26
Q

Name the GABA ionotropic receptors and the GPCR G-proteins they couple to.

A

GABAb receptors = couples to Gi and Go proteins

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27
Q

How many subunits does a glutamate ionotropic receptor have?

A

4

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28
Q

How many subunits does a GABA ionotropic receptor have?

A

5

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29
Q

What specific binding site is found on the GABAa ionotropic rector?

Is this the same binding site as the one GABA binds to?

What drugs act here?

How do these drugs therefore achieve their effects?

A

Benzo binding site = different to GABA binding sites

Benzodiazepines = midazolam, diazepam, lorazepam

These drugs are positive allosteric modulators = help GABA do their job = calming effect (as GABA is inhibitory in CNS)

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30
Q

What transporters are involved with the reuptake of GABA?

A

GAT1 = neuronal GABA transporter

GAT3 = glial cell (astrocyte) GABA transporter

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31
Q

Where is most GABA degraded?

What enzyme and reaction carries this out?

A

GABA —> succinyl semialdehyde

GABA transmaminase = enzyme = same that turns alpha-oxogluterste into glutamate in glial cells

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32
Q

Name some PAM (positive allosteric modulators) of the GABAa receptor?

A

Benzodiazepines

Ethanol

Propofol

Barbiturates

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33
Q

What is baclofen used for?

How does it work?

A

MS type diseases

GABAb metabotropic receptor agonist

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34
Q

Name 2 Ach receptor types?

Which is ionotropic and which is metabotropic?

A

Muscarinic (metabotropic = remember ‘M’ for ‘M’)

Nicotinic = ionotropic

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35
Q

Explain the somatic motor pathway in terms of its neurons and NT’s at the neuromuscular junction.

A

Cell body is in the CNS, travels straight (without synapsing) to the muscle

Releasese Ach onto nicotinic receptors

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36
Q

Explain the parasympathetic pathway in terms of its neurons and NT’s both pre and post ganglionic.

A

Pre-ganglionic = releases Ach onto Nicotinic receptors

Post-ganglionic = releases Ach onto Muscarinic receptors

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37
Q

What 3 main nuclei are Ach found?

A

Nucleus basalis = projects to whole cortex = dies early in Alzheimer’s

Septo-hippocampal pathway

Substantia nigra thalamus pathway

Small striatal pathways = Parkinson’s

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38
Q

How is Ach synthesised?

A

Choline (diet) + Acetyl-CoA (krebs cycle) = Ach

Enzyme = Choline Acetyltransferase (ChAT)

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39
Q

Where is Ach synthesis carried out?

Where is ChAT synthesis carried out?

A

Ach = at nerve terminal

ChAT = at cell body and transported to nerve terminal

40
Q

How is Ach stored?

How is this achieved?

What is the transporter called that achieves this?

A

In vesicles

Same process as Glutamate and GABA (proton pump and H ion anti-porter)

Transporter = called VAchT (vesicular Ach transporter)

41
Q

How does Ach release work?

A

Same as GABA and Glutamate = calcium dependant vesicular release

42
Q

What are the subunits of a muscle nAChR?

A

X2 alpha 1’s
X1 beta 1
X1 delta
X1 epsilon

43
Q

What are the subunits of a neuronal nAChR?

Are others available?

A

X2 alpha 3’s
X3 beta 4’s

Yes

44
Q

How many subunits do nAChR receptors have?

A

5 = pentameric

45
Q

How many and what are the names of Ach muscarinic recpetors?

What type of receptors are these?

What G-protein are each associated with?

A

M1-5

Metabotropic GPCR receptors

Odd (1,3,5) associated with Gq and GII

Even (2,4) associated with Go and Gi

46
Q

Can Ach be reuptaken?

A

Yes but must be degraded to choline first by acetylcholinesterase

No Ach transporter!

47
Q

How does botulinus toxin work?

What effect does this have?

A

Interrupts Ach release (vesicles recognition of membrane for exocytosis = SNARE proteins)

Therefore causes paralysis as Ach can not be released

Cosmetic = relaxation of muscles and wrinkle disappearance

48
Q

How does Sux work?

What kind of drug is it?

A

Normally Ach released, quickly acts on post-synaptic nAChR’s then degraded (hydrolysed) by acetylcholinesterase, with the post-synaptic cell being repolarised

Sux = Ach nicotinic agonist = therefore DEPOLARISING muscle relaxant

Longer duration than Ach = NOT hydrolysed by acetylcholinesterase, maintains membrane potential above threshold (keeps it depolarised)

Calcium is taken up by SR independently of membrane repolarization therefore flaccidity not tetany post-fasciculations

49
Q

Name a drug used for smoking cessation linked to the Ach nicotinic receptors and explain how it works.

A

Champix = partial Ach nicotinic receptor agonist

Combats the addiction by stimulating receptors (partially)

Inihibits nicotine from binding to some degree

Therefore good for cessation and addiction

50
Q

How do pancuronium and vecuronium work?

A

Reversible antagonists of nicotinic Ach receptors

51
Q

How do ipitropium and atropine work?

A

They are reversible antagonists of the mACh receptors

Therefore inhibits parasympathetic = inhibits bronchoconstriction and bradycardia

52
Q

How does Neostigmine work?

A

Blocks AchE enzyme from breaking down Ach

Therefore it is used for non-depolarising muscle relaxation reversal

53
Q

In Alzheimer’s dementia, what NT level is low?

How do dementia drugs therefore work?

Name some.

A

Ach

Drugs are therefore cholinesterase inhibitors which aim to increase Ach levels in the brain

Rivastigmine, donepezil, galantamine, tacrine

54
Q

How is myesthenia gravis linked to Ach?

A

Autoimmune disease where autoantibodies attack nAChR

55
Q

What are the nuclei and pathways where dopamine acts?

A

Nigrostriatal = substantia nigra nuclei = first pathway affected in Parkinson’s

Mesolimbic pathway (hippocampus and amygdala)

Mesocortical pathway (forebrain)

Tubero-hypophyseal pathway (hypothalamus and pituitary)

56
Q

How is dopamine synthesised?

A

Tyrosine = diet
DOPA (tyrosine hydroxalase)
Dopamine (dopa decarboxylase)

57
Q

How is dopamine stored?

How is it transferred to this place of storage?

A

In vesicles

Places there by VMAT transporters (vesicular monoamine transporters) V1 and V2

Driven by hydrogen ion gradient caused by a separate proton pump (same as glutamate, GABA, Ach)

58
Q

How is dopamine released?

A

Same as others

Calcium dependant vesicular release

BUT!

Varicosities along axon allow dopamine release along axon, not just at end terminal!!

59
Q

What 2 french names are given to both NT release at end terminals and along axons?

A

End terminal = end terminal “Bousant”

Along axon = “en passant” varicosity

60
Q

What types of dopamine receptors are there and how are they named?

A

GPCR Metabotropic only!

D1 like = D1 and 5 = coupled to Gs

D2 like = D2, 3 and 4 = coupled to Gi

61
Q

How is dopamine reuptaken?

A

DAT (dopamine active transporter)

62
Q

There are multiple pathways of degradation of dopamine, but what is the end degraded product (that would be measured if needed)?

A

Homovanillic acid

63
Q

What are the major NT’s at play in:

1) Alzheimer’s
2) Parkinson’s

A

1) Ach

2) Dopamine

64
Q

What is levodopa and how does it work?

A

Parkinson’s drug

Crosses blood brain barrier whereas dopamine can not

Elevated dopamine levels to combat Parkinson’s effects

65
Q

What drugs interfere with dopamine storage?

A

Reserpine, methamphetamine

66
Q

How does haloperidol work and what does it do?

A

It is an antipsychotic

It is a dopamine receptor antagonist

67
Q

What does cocaine cause and how?

A

It is a stimulant, it causes euphoria by blocking dopamine reuptake, increasing levels in the synaptic cleft

68
Q

What drug is given in combination with L-DOPA and how does it work?

A

Selegiline - MAO inhibitor = acts to increase dopamine levels

69
Q

Is Alzheimer’s more common in men or women?

By how much?

A

Women X2 more likely = 1/5

Men 1/10

70
Q

What 2 hisopathological changes are seen in Alzheimer’s?

A

Amyloid deposits form plaques outside of neuronal cells

Hyperphosphorylated tau proteins form neurofibrillary tangles inside neuronal cells

71
Q

What structure is the precursor of amyloid plaques seen in Alzheimer’s?

Where is it found and what is its function?

A

Amyloid precursor protein

It spans the neuronal cell membrane and helps with repair and growth

72
Q

When APP is used it is broken down. What molecules break this down and how can this lead to amyloid plaques?

A

Alpha and gamma secratases = normal

BETA and gamma secratases = formation of amyloid plaques outside of cells as left over fragment (amyloid BETA(!)) is not soluble

73
Q

What are tau proteins and how can they misfunction in Alzheimer’s?

A

Tau = structural proteins on neurones

Can because hyperphosphorylated and tangles (neurofibrillary tangles)

74
Q

What gross structural changes occur in Alzheimer’s to the brain?

A

Gyri narrowing

Sulci deepening

Ventricles enlarging

75
Q

Are the majority of Alzheimer’s cases sporadic or familial?

By what percentage?

What is the onset difference with each?

What genes are associated with each?

A

Sporadic = 90-95% = Apiloprotein E e4 (APOE-e4) gene = late onset

Familial = 5-10% = Presenilin 1 (chromosome 14), 2 (chromosome 1) and APP (chromosome 21) genes = early onset

76
Q

What does APOE-e4 do and why is it bad for Alzheimer’s risk?

A

APOE = breaks down beta amyloid = e4 variant poor at doing so therefore risk increases

77
Q

What is the inheritance pattern of familiar Alzheimer’s?

A

Autosomal dominant (chromosome 21 = APP gene)

78
Q

What are the NT theories in Alzheimers?

Which drugs act on each theory to help treat Alzheimer’s?

A

1) Cholinergic neurones lost first = Ach levels drop = memory and cognition loss

Drugs therefore anticholinesterases = donepezil, rivastigmine, galantamine

2) Glutamate in Alzheimer’s disease because too high and causes excitotoxicity where cells are too highly stimulated and may die as a result (only if not synaptic receptors)

Drugs therefore = MEMANTINE = competitive antagonist of NMDA receptor (extra-synaptic specific)

79
Q

Name some prodromal symptoms of Parkinson’s?

A

Constipation (dopaminergic loss in enteric NS)

Smell changes = anosmia(olfactory)

80
Q

Which brain areas are affected in dementia?

A

Hippocampus first = short term memory loss

Later = widespread to cortex = longer term memory loss and other motor symptoms associated

81
Q

Which brain areas are affected in parkinsons?

A

The pars compacta part of the substantia nigra

The nigra-striatal pathway is therefore affected

Corpus striatum = caudate nucleus + putamen

Movement therefore affected = as seen with Parkinson’s

82
Q

Explain the role of Ach in the enteric NS of parkinsons patients.

Why can drugs that affect Ach have a beneficial effect on Parkinson’s patients?

What drugs are therefore detrimental to Parkinson’s patients?

A

Ach key in gut motility

Dopine lathways in ENS die in parkinsons = they get constipation

AchE inhibitors (rivastigmine, donepezil) can increase available Ach in the gut and help with constipation

They also help dopa drugs with absorption so are beneficial

Anti-cholinergic drugs therefore bad for Parkinson’s patients

83
Q

Name some Parkinson symptoms.

A 
Bradykinesia (slow movements)
Tremor (resting) in limbs
Rigidity
Shuffling gate
Dysphagia
Constipation
Anosmia
84
Q

Do Parkinson’s motor signs start uni or bilaterally?

A

Unilaterally and progress bilaterally

85
Q

Is dopamine the only NT affected in Parkinson’s?

A

No, all 3 NT’s affected:

  • Dopamine
  • -
86
Q

Which conditions involve Lewy bodies?

What are they?

A

Parkinson’s and dementia with Lewy bodies

They are protein aggregates (alpha-synuclein)

87
Q

An exposure of what may increase risk of Parkinson’s?

A

Pesticides

88
Q

What does Parkinson’s do to power?

A

Nothing! Power not affected, no weakness seen

89
Q

What drug is given with L-Dopa and why?

A

Carbidopa = dopa decarboxylase inhibitor

Does not cross BBB (blood brain barrier)

Dopa decarboxylase converts L-Dopa to Dopamine in the periphery therefore stopping it crossing the BBB to take effect, cabidopa therefoee prevents this

90
Q

What does amatadine do?

What kind of drug is this?

A

Increases dopamine production

An anti-viral

91
Q

What is the name of the 2 dopamine degradation enzymes/pathways?

A

MAO

COMT

92
Q

What do Parkinson style drawing (e.g. spirals) look like?

A

Micrographia = small = rest tremor

If drawing looks like tremor occurred = intention tremor = not Parkinsonian

93
Q

Name some COMT inhibitors.

A

Entacapone

Tolcapome

94
Q

Name some MOA inhibitors.

A

Selegilene

95
Q

Other than dopamine, what other NT’s are treated and how?

A

Dopamine is low

Ach therefore is RELATIVELY high

Anti-cholinergics therefore given

96
Q

What scan is useful in Parkinson’s and what may it show if positive?

A

DaTSCAN

Comma shape —> full stop shape on affected side

97
Q

Name a transdermal patch used in Parkinson’s and how does it work?

A

Rotigotine = dopamine receptor agonist

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