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Neurotransmitters Flashcards

1
Q

Glutamate role in CNS

A

excitatory neurotransmitter (balance with GABA)

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2
Q

Glutamate receptors

A

Ionotropic - AMPA (4), NMDA (5), kainate (5)
Metabotropic

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3
Q

Metabotropic glutamate receptors

A

Gaq
regulation on presynapse
I - III

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4
Q

Kainate receptors

A

Na+

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5
Q

AMPA receptors

A

Na+

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6
Q

NMDA receptors

A

Ca2+ (N-methyl-D-aspartate)
Too much Ca2+ can cause cell death processes and proteases to enter cell

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7
Q

Glutamate receptor agonists

A

glutamate, aspartate, kainate, quisqualate, AMPA (synthetic)

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8
Q

Sodium influx with different ligands

A

some stronger than others eg demoate stronger than kainate

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9
Q

Glutamate receptor antagonists

A

CNQX
GYKI-52466 - blocks AMPA

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10
Q

effect of glutamate subunit composition

A

different distribution throughout brain
changes the duration and intensity of kainate and AMPA signalling

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11
Q

NMDA subtypes

A

GluN-1 obligatory for function
2A and B regulate
C and D kinetics
3A and 3B not strongly expressed in adults

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12
Q

Co-localisation

A

AMPA and NMDA -> learning and memory
LTP and LTD (long term depression) changes receptor concentration

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13
Q

High frequency vs low frequency glutamate release

A

Low - not much NMDA activation (LTD)
High - NMDA unblocked, efficacy remains
D-APV is NMDA antagonist - stops spatial memory

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14
Q

Glutamate therapeutic potential

A

schizophrenia, depression, epilepsy and heart disease

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15
Q

GABA role

A

major inhibitory neurotransmitter mainly in brain tissue

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16
Q

GABA formation

A

Glutamate + glutamic acid decarboxylase

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17
Q

GABA reuptake/metabolism

A

GABA-transaminase

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18
Q

GABAa

A

ionotropic
pentamers - mainly alpha (6), beta (4), gamma (3) subunits (a1,b2,y2 common)
Causes hyperpolarisation
High density in neocortex but everywhere

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19
Q

GABAb

A

metabotropic (GPCRs)
B1a and b, B2 - need both
adenylate cyclase coupled
pre (decrease Ca2+) and post synapse (increase K+)

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20
Q

GABA drugs

A

benzodiazepines, anaesthetics, barbituates, alcohol, anticonvulsants
GABAb - antispasticity

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21
Q

GABA in fetus development

A

Excitatory
NKCC1 - pull Cl- into cell
GABAa - reversed (Cl- out of cell) = excitation

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22
Q

tinnitus

A

acoustic trauma in the cochlea nucleus

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23
Q

benzodiazepines

A

bind to GABAa subunit gamma2 required for response
increase Cl- influx (PAM)
only if GABA present

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24
Q

Propophol

A

anaesthetic alpha2, beta3, gamma2 selective
beta3 crucial

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25
Flumazenil
treat benzodiazepines overdose antagonist/NAM (may be inverse agonist) pro-convulsant and increase anxiety
26
baclofen
GABAb agonist bad side effects stereoisomers - (L) works with tinnitus treat drug dependance
27
GABAc
ionotropic p1-3 30% same as GABAa
28
Serotonin
5-hydroxytryptamine, monoamine, 14 receptors Produced by enterochromaffin cells in intestine wall and platelets in serum or centrally by neurons (lots from raphe nuclei)
29
Serotonin receptors
GPCRs, 5-HT1-7, 5HT-1B = presynapse (regulatory, desensitisation) 5-HT3 = ligand gated ion channel (5 subunits x 4 transmembrane domains) 5-HT1 = whole CNS (Gi)
30
Serotonin transport
SERT 12 transmembrane domains, clear from synaptic cleft via Cl-/Na+ exchange
31
Serotonin degradation
Monoamine oxidase (MAO) Mostly A
32
Unipolar depression
Deficiency of NA and 5HT (more complex than that) Evidence = DL-fenfluramine serotonin releasing drug limited response and PET scanning Against = not enough evidence, bad experiments, no big effects via antidepressants
33
Antidepressants
Non-selective inhibitors of monoamine uptake MAOIs, SSRIs, SNRIs Mianserin, trazodone, mirtazapine
34
SSRIs
Better side effect profile (nausea, vomiting, sexual dysfunction, diarrhoea, constipation) Can take up to two weeks to work
35
Tricyclic antidepressants
Block reuptake 5-HT, NA Also AChR, a-NA R, histamine receptors
36
MDMA
Structurally similar to methamphetamine Blocks serotonin reuptake by transporter - caused transporter to release serotonin MDA metabolite causes neurotoxicity Chronic effects = synapses degrade, less transporter Adverse events a bit funky due to bad animal -> human dose calculations
37
Dopamine
Precursor of NA and A, monoamine and catecholamine Degraded by MAOa and MAOb and COMT
38
Monoamine synthesis pathway
Tyrosine -> DOPA -> Dopamine -> NA -> Adrenaline
39
Dopamine pathways in brain
Substantia nigra -> basal ganglia (nigrostriatal pathway) Tegmentum -> nucleus accumbens + frontal cortex (mesolimbic, mesocortical) Hypothalamus (tuberinfundibular)
40
Parkinsons
Loss of substantial nigra neutrons = 90% lost at basal ganglia (nigrostriatal pathway), increased effect of ACh Tremor, rigidity, bradykinesia, loss of balance, shuffling, reduced arm movement, facial expressions Idiopathic = irreversible and unknown cause, disappearance of dark melanin-containing neurons of SNC, Lewy bodies
41
Schizophrenia
Too much dopamine at frontal cortex/nucleus accumbens (mesolimbic and mesocortical)
42
Dopamine receptors
D1 family = D1 (striatum and neocortex) and D5 (hippocampus and striatum), increase cAMP, inhibit K+, effect on Ca2+, enhance NMDA D2 family = D2, D3 and D4, decreae cAMP, increase K+, inhibit Ca2+ (striatum, hippocampus, cortex/nucelus accumbens)
43
Parkinsons drugs
Increase dopamine synthesis = L-Dopa Increase dopamine release = Amantadine Activate dopamine receptors = bromocriptine Prevent dopamine metabolism = selegiline Balance ACh and dopamine = trihexyphenidyl
44
L-Dopa
Levodopa Precursor for dopamine, rapid breakdown, used for Parkinson's as treats bradykinesia and rigidity Combined with carbidopa to reduce peripheral side effects Need functioning dopamine synapses, only 1% goes to the brain, what is in the brain is degraded by MAOb and COMT Side effects = nausea, vomiting, cardiovascular, hallucinations, confusion Decreased efficacy after 5 years, on-off phenomenon
45
Selegiline
Selective, irreversible MAOb inhibitor Slightly effective on its own in early PD, may retard progression of disease
46
Bromocriptine and Ropinirole
Long half life, reduce dose of L-dopa and control on-off phenomenon Bromocriptine - D2 receptor agonist (GI effects, hypotension, dyskinesia) Ropinirole - D2, D3, D4 agonist (somnelence, syncope, hypotension, hallucinations, dyskinesia
47
Anti-muscarinics for PD
Benzatropine May improve tremor and rigidity but no effect on bradykinesia Dry mouth, blurred vision, constipation, anorexia, confusion, sedation
48
Scizophrenia
Type 1 - positive symptoms - delusions, paranoia, auditory hallucinations, disorders of thought, inappropriate behaviour Type 2 - negative symptoms - social withdrawal, apathy, cognitive impairment Tegmentum to neocortex Excess of dopamine, release dopamine = induce psychosis (mesolimbic and mesocortical pathways)
49
Schizophrenia drugs
Reduce DA synthesis Reduce DA release Block D2 receptors Increase DA metabolism
50
Classical antipsychotics
D2 antagonists Chlorpromazine, flupentixol, haloperidol High therapeutic index, lag 1-2 weeks Sedation, anticholinergic side effects, extrapyramidal side effects Potency/affinity balances sedation and extrapyramidal effects (Halo high)
51
Atypical antipsychotics
No extrapyramidal symptoms, works for negative symptoms, refractory schizophrenia Clozapine, risperidone, quetiapine, remoxipride
52
Clozapine
Weak D2 antagonist (also 5HT2a and D4) Withdrawn due to reduced white blood cell count then reintroduced Effective for 60% of refractory patients Sedation, tachycardia, dizziness, seizures
53
Risperidone
5HT2 antagonist and D2 More effective than haloperidol, similar efficacy clozapine Long acting, slow release options Sedation, difficulty concentrating
54
Quetiapine
Antagonist at 5-HT2a and D2 positive and negative symptoms and dipolar mania somnolence, dizziness, dry mouth, weight gain, some extrapyramidal symptoms
55
Remoxipride
Weak, selective D2 antagonist (exrastriatal receptors) Similar to haloperidol Low incidence extrapyramidal symptoms Insomnia, tiredness, tremor, difficulty concentration, akathisia
56
Other causes for schizophrenia
Glutamatergic dysfunction, NMDA receptors
57
Other causes for schizophrenia
Glutamatergic dysfunction, NMDA receptors
58
Acetylcholine
Made form Acetyl CoA via choline acetyltransferase (and coenzyme A) in presynapse Broken down in synaptic cleft by acetylcholine esterase which is on the post-synapse Neurons from nucleus basalis and in septohippocampal pathway
59
Nicotonic ACh receptors
Ligand gated ion channels 5 subunits with 4 transmembrane domains alpha 1-9, beta 1-4 plus gamma, delta, epsilon (a4, B2 high) Can be homomeric (alpha, high affinity nicotine) or heteromeric (alpha and beta, low affinity nicotine) different subtypes have different polarisation
60
Epibatidine
Alkaloid found on Ecuadorian frog AChE inhibitor, agonist nAChR, antagonist mAChR analgesia, muscle paralysis,
61
Anatoxin
nAChR agonist, not degraded by AChE lose coordination, convulsions, respiratory paralysis Depolarising block
62
Sarin
Organiphosphorous, inhibits AChE Paralysis and death
63
Muscarinic ACh receptors
M1-M5, GPCRs Muscarine/pilocarpine = selective Atropine and hyoscine = non-selective antagonist (effect on forgetting) Phigostigmine = anticholesterase, elevate levels
64
Alzheimers
60% increased risk of dementia Hearing loss, loss of sensory imput, less stimulation Biomarkers = neuronal loss in medial temporal lobe, amyloid plaques - B-amyloid, neurofibrillary tangles
65
Alzheimers treatment
Donezepil - reversible, selective AChE inhibitor (and rivastigmine, galastigmine), is not very effective, expensive Tacrine - doesn't last, remain at home Galantaine - palliative responders

PHAL303 (8 decks)

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