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PHAL303 > Neurotransmitters > Flashcards

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
Q

Flumazenil

A

treat benzodiazepines overdose
antagonist/NAM (may be inverse agonist)
pro-convulsant and increase anxiety

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26
Q

baclofen

A

GABAb agonist
bad side effects
stereoisomers - (L) works with tinnitus
treat drug dependance

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27
Q

GABAc

A

ionotropic
p1-3
30% same as GABAa

28
Q

Serotonin

A

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
Q

Serotonin receptors

A

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
Q

Serotonin transport

A

SERT
12 transmembrane domains, clear from synaptic cleft via Cl-/Na+ exchange

31
Q

Serotonin degradation

A

Monoamine oxidase (MAO)
Mostly A

32
Q

Unipolar depression

A

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
Q

Antidepressants

A

Non-selective inhibitors of monoamine uptake
MAOIs, SSRIs, SNRIs
Mianserin, trazodone, mirtazapine

34
Q

SSRIs

A

Better side effect profile (nausea, vomiting, sexual dysfunction, diarrhoea, constipation)
Can take up to two weeks to work

35
Q

Tricyclic antidepressants

A

Block reuptake 5-HT, NA
Also AChR, a-NA R, histamine receptors

36
Q

MDMA

A

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
Q

Dopamine

A

Precursor of NA and A, monoamine and catecholamine
Degraded by MAOa and MAOb and COMT

38
Q

Monoamine synthesis pathway

A

Tyrosine -> DOPA -> Dopamine -> NA -> Adrenaline

39
Q

Dopamine pathways in brain

A

Substantia nigra -> basal ganglia (nigrostriatal pathway)
Tegmentum -> nucleus accumbens + frontal cortex (mesolimbic, mesocortical)
Hypothalamus (tuberinfundibular)

40
Q

Parkinsons

A

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
Q

Schizophrenia

A

Too much dopamine at frontal cortex/nucleus accumbens (mesolimbic and mesocortical)

42
Q

Dopamine receptors

A

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
Q

Parkinsons drugs

A

Increase dopamine synthesis = L-Dopa
Increase dopamine release = Amantadine
Activate dopamine receptors = bromocriptine
Prevent dopamine metabolism = selegiline
Balance ACh and dopamine = trihexyphenidyl

44
Q

L-Dopa

A

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
Q

Selegiline

A

Selective, irreversible MAOb inhibitor
Slightly effective on its own in early PD, may retard progression of disease

46
Q

Bromocriptine and Ropinirole

A

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
Q

Anti-muscarinics for PD

A

Benzatropine
May improve tremor and rigidity but no effect on bradykinesia
Dry mouth, blurred vision, constipation, anorexia, confusion, sedation

48
Q

Scizophrenia

A

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
Q

Schizophrenia drugs

A

Reduce DA synthesis
Reduce DA release
Block D2 receptors
Increase DA metabolism

50
Q

Classical antipsychotics

A

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
Q

Atypical antipsychotics

A

No extrapyramidal symptoms, works for negative symptoms, refractory schizophrenia
Clozapine, risperidone, quetiapine, remoxipride

52
Q

Clozapine

A

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
Q

Risperidone

A

5HT2 antagonist and D2
More effective than haloperidol, similar efficacy clozapine
Long acting, slow release options
Sedation, difficulty concentrating

54
Q

Quetiapine

A

Antagonist at 5-HT2a and D2
positive and negative symptoms and dipolar mania
somnolence, dizziness, dry mouth, weight gain, some extrapyramidal symptoms

55
Q

Remoxipride

A

Weak, selective D2 antagonist (exrastriatal receptors)
Similar to haloperidol
Low incidence extrapyramidal symptoms
Insomnia, tiredness, tremor, difficulty concentration, akathisia

56
Q

Other causes for schizophrenia

A

Glutamatergic dysfunction, NMDA receptors

57
Q

Other causes for schizophrenia

A

Glutamatergic dysfunction, NMDA receptors

58
Q

Acetylcholine

A

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
Q

Nicotonic ACh receptors

A

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
Q

Epibatidine

A

Alkaloid found on Ecuadorian frog
AChE inhibitor, agonist nAChR, antagonist mAChR
analgesia, muscle paralysis,

61
Q

Anatoxin

A

nAChR agonist, not degraded by AChE
lose coordination, convulsions, respiratory paralysis
Depolarising block

62
Q

Sarin

A

Organiphosphorous, inhibits AChE
Paralysis and death

63
Q

Muscarinic ACh receptors

A

M1-M5, GPCRs
Muscarine/pilocarpine = selective
Atropine and hyoscine = non-selective antagonist (effect on forgetting)
Phigostigmine = anticholesterase, elevate levels

64
Q

Alzheimers

A

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
Q

Alzheimers treatment

A

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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