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NSB Lectures > Chemicals in the brain > Flashcards

Chemicals in the brain Flashcards

1
Q

What is the life cycle of neurotransmitters?

A

AP in presynaptic fiber
Synthesis of transmitter
Storage
Metabolism
Release
Reuptake
Degradation
Receptor (agonists/antagonists)
Receptor induced increase or decrease in ionic conductance
Retrograde signalling
Second messengers

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2
Q

Are neurotransmitters endo or exogenous?

A

endogenous

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3
Q

Are neurotransmitters released intra or extracellularly?

A

extracellularly

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4
Q

Which neurotransmitters are under the chemical class of amino acids?

A

Glutamate
Aspartate
GABA
Glycine

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5
Q

Which neurotransmitters are under the chemical class of monoamines?

A

Dopamine
Noradrenaline
Adrenaline
Serotonin

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6
Q

ACh is an ester of what?

A

acetic acid and choline

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7
Q

What is the life cycle of neurotransmitter?

A

Synthesis
Storage
Vesicle transport and fusion with membrane
Release
Diffusion across synaptic cleft
Action on post-synaptic cell
Signal termination

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8
Q

Do inhibitory neurotransmitters hyperpolarise or depolarise membranes? Which ion does this directly effect?

A

Hyperpolarise - makes cell more stable
Cl-

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9
Q

Do excitatory neurotransmitters hyperpolarise or depolarise membranes?

A

Depolarise
Na+

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10
Q

What is the major inhibitory amino acid?

A

GABA

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11
Q

What is the primary excitatory amino acid?

A

Glutamate

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12
Q

Are amino acids located in a specific area of the brain?

A

No - ubiquitous distribution

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13
Q

Is glutamate sourced or synthesised?

A

Both - sourced from diet and synthesised from a-ketoglutarate and glutamine

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14
Q

Glutamate is sequestered into synaptic vesicles via what?

A

Vesicular glutamate transporters (VGLUTS)

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15
Q

Glutamate is released into synaptic vesicles when an AP arrives where?

A

synaptic bouton

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16
Q

What processes are affected by glutamate?

A

Pain sensation
Cerebral neurotoxicity
Memory

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17
Q

What type of receptors does Glutamate have?

A

Ionotropic (NMDAr, AMPAr, Kainate)
Metabotropic (ACPD; mGlu)

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18
Q

What mediates a small amount of glutamatergic transmission?

A

metabotrophic receptors (mGlu)

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19
Q

What ions are the majority of AMPA receptors permeable to?

A

Na+ + K+

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20
Q

What ions are all NMDA receptors highly permeable to?

A

Ca2+, Na+ + K+

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21
Q

NMDA receptors have a blockade of what?

A

Mg2+

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22
Q

What needs to happen to AMPA before glutamate can act on NMDA receptors?

A

Glutamate acts on AMPA receptors to depolarise cell

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23
Q

What needs to happen to stop Mg2+ from blocking NMDA receptors?

A

Glutamate and glycine binding and strong depolarisation = removal of Mg2+ and rise in intracellular Ca2+

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24
Q

What is ‘wind up’?

A

Persistent pain signal causes a continued increase of Ca2+ through NMDA receptors, increasing transcription of more glutamate receptors.
Then can causes oxidative stress, gene transcription, altered synaptic morphology and cell death

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25
What is excitotoxicity?
Neuronal damage/death caused by excessive cellular excitation. Pathophysiologic mechanism; stroke, epilepsy
26
Do NMDA and AMPA receptors only get activated by Glutamate?
No AMPA - Alcohol, anaesthetics NMDA - Phencyclidine
27
How is glutamate recycled through neighbouring cells and why?
Glutamate sequestered from synaptic space by transport molecules on membrane of presynaptic neurone + neighbouring glial cells. Glutamate taken back up into glutamatergic neurones (Gt(n) transporters), broken down to glutamine, packed into vesicles to then be used again in glial cells when converted back to glutamate. Protective mechanism.
28
Which drug used in Alzheimers acts as a noncompetitive NMDA antagonist?
Memantine
29
What are the functional associations of GABA?
Arousal and attention Memory formation Anxiety Sleep Muscle tone
30
What is GABA synthesised from?
Glutamate within GABAergic neurones
31
GABA is sequestered into synaptic vesicles by what?
GABA transporter
32
Which GABA receptor is ionotropic (fast) and has an integral Cl- channel?
GABA A
33
Which GABA receptor is metabotropic (slow), has seven transmembrane domains and is G-protein linked (due to opening of K+ channels)?
GABA B
34
Which GABA receptor is ionotropic and has a transmitter gated Cl- channel?
GABA C
35
Which GABA receptor does the majority of GABAergic transmission work through?
GABA A
36
What is the Ecl in neurones?
-70mV
37
When GABAergic nerve fibres are stimulated, where does the Em (membrane) move closer to? Does this make the cell more of less excitable?
Ecl Less excitable
38
GABA is taken back up by what?
Glial cells (via GAT 1/2/3)
39
Once GABA is taken up by glial cells, what is it converted to?
Glutamate -> Glutamine -> enters GABAergic neurones -> converted to glutamate -> GABA -> Packaged into vesicles
40
What are the four main monoamines?
Dopamine Noradrenaline Adrenaline Serotonin
41
What is the synthesis of dopamine, noradrenaline and adrenaline?
Tyrosine -> L-DOPA -> Dopamine -> Noradrenaline -> Adrenaline
42
Which enzyme converts L-DOPA to dopamine?
Aromatic Amino acid Decarboxylase
43
What is serotonin synthesised from?
Tryptophan
44
Can serotonin be synthesised further?
Yes - into melatonin
45
Which dopamine receptors are G-protein linked?
All - D1-D5
46
What is the MoA of 'D1 family' receptors?
D1+D5, increase cAMP through Gs
47
What is the MoA of 'D2 family' receptors?
D2, D3 + D4, decrease cAMP through Gi
48
Where are D1 + D2 receptors present?
Postsynaptically in the striatum
49
Which dopamine receptor functions as an autoreceptor?
D2
50
Where are D4 receptors present?
In the cortex, not striatum.
51
Which dopamine pathway controls movement?
Nigrostriatal
52
Which dopamine pathway controls emotion, reward system/addiction?
Mesocorticolimbic
53
What three things can be done to Dopamine to help Parkinson's disease symptoms?
Augmentation of dopamine (increase synthesis) Dopamine agonists Inhibit dopamine metabolism
54
What drug class can treat nausea and schizophrenia?
Dopamine antagonists
55
Which receptors mediate the effects of NA + Adr in the CNS?
a and b adrenoceptors
56
Presynaptically, which adrenoceptor modulates NA release + the rate of firing of noradrenergic neurones?
a2
57
When drugs act to increase brain NA, what effect does this have on forebrain B-adrenoceptors?
down regulates
58
For a drug to get to the CNS, does it have to go through the PNS?
yes
59
Where do a-adrenoceptors act?
Blood vessels of organs and tissues except skeletal muscle vessels
60
Which drugs are a-adrenoceptor agonists?
NA, Adr, Isoprenaline
61
Which drugs are a-adrenoceptor antagonists?
Phentolamine
62
Where do B1 B-adrenoceptors act?
Myocardium
63
Where do B2 B-adrenoceptors act?
Bronchi, uterus, muscle + coronary vessels
64
Where to B3 B-adrenoceptors act?
Adipose tissue
65
What drugs are B-adrenoceptor agonists?
NA, Adr + Isoprenaline
66
What drugs are B-adrenoceptor antagonists?
Propanolol
67
Are a or b adrenoceptors sensitive to up/down regulation?
B
68
What are the functional associations of NA?
Arousal + increased attention Facilitates responsiveness of brain regions to other neurotransmitter systems
69
In terms of pharmacology, how are depression and affective disorders generally treated?
Block reuptake of NA (Tricyclic, Serotonin + NA reuptake inhibitors) Inhibition of degradation of NA
70
How does cocaine affect NA?
Blocks its reuptake
71
How do amphetamines affect NA?
Increases its release
72
What is the chemical name of serotonin?
5-HT
73
How are second messengers signalled by 5-HT?
Use of G-protein, except for 5-HT3
74
Which 5-HT receptor subtype acts as an autoreceptor?
5-HT1A
75
Are most 5-HT receptors located pre or post synaptically?
post
76
Where are serotonergic nuclei located?
In the raphe nuclei in the brainstem
77
What are the functional associations of 5-HT?
Send descending fibres to spinal cord to inhibit input from nociceptive pathways (descending control of pain) Send fibres in medial forebrain to forebrain structures + cerebral blood vessels (migraine)
78
What can diminished serotonergic transmission lead to?
Depression
79
What drugs are first line for depression?
SSRIs
80
What does MDMA increase the release of?
5-HT
81
What is the main way monoamines are terminated?
Reuptake via plasma membrane transporters in pre-synaptic neuron
82
Apart from reuptake, how else are monoamines terminated?
Uptake by non-neuronal cells. Metabolism of endogenous + exogenous DA, NA, Adr + 5-HT (exo small amount left in cleft, then broken down) by MAO A/B + COMT. Blockade of monoamine transporters + degradative enzymes (MAO) = increased concentrations of monoamines in synapse or neurone.
83
Which enzyme metabolises dopamine in the cytosol?
MAO-B
84
Which enzyme metabolises dopamine in the cleft?
COMT
85
Which enzyme metabolises NA?
MAO-A
86
Which enzyme metabolises serotonin?
MAO-A
87
What is ACh synthesised by?
Choline acetyltransferase
88
What is ACh made from?
Choline + Acetyl CoA
89
What is ACh broken down by in the synaptic cleft?
Acetylcholinesterase (AChE) or Butyrylcholinesterase (BuChe)
90
Once ACh is broken down, what happens to choline?
Transported back to axon terminal to make more ACh
91
What are the receptors of ACh?
Nicotinic or Muscarinic
92
Which ACh receptor is excitatory?
Muscarinic + Nicotinic Muscarinic can also be inhibitory
93
What is choline stored as?
Phosphorylcholine in phospholipids. Phosphatidylcholine in plasma
94
Can ACh be reuptaken?
No, broken down by AChE into choline + acetate. Choline uptake into synapse
95
What is Acetyl CoA derived from?
Glycolysis
96
What is the MoA of muscarinic receptors?
Metabotropic (G protein)
97
Where are muscarinic receptors located?
Postsynaptically in smooth muscle, cardiac muscle + glands
98
What are agonists of Muscarinic receptors?
ACh + Muscarine
99
What are antagonists of muscarinic receptors?
atropine (belladonna)
100
What MoA do nicotinic receptors have?
Ionotropic (pentameric cations channel)
101
Where are nicotinic receptor located?
Autonomic ganglia, motor endplate + CNS
102
What are agonists of nicotinic receptors?
ACh + nicotine
103
What are antagonists of nicotinic receptors?
Curare (Tubocurarine)
104
What are some functional associations with ACh?
Cognition, memory, attention, pain suppression, neural plasticity. Neuromodulation Long term-potentiation.
105
What can ACh be used to treat?
Motion sickness Neuromuscular diseases (Myasthenia gravis) Acute neuromuscular blockade and reversal Dystonias + headaches Symptoms of Alzheimers, cognitive dysfunction

NSB Lectures (48 decks)

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