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BMS2002 > strand 1 > Flashcards

strand 1 Flashcards

1
Q

SCN9A

A

gene linked to human pain perception
mutations> channelopathies

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2
Q

secondary active transport

A

indirect coupling molecule with another moving along echem gradient
antiport/ symport

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3
Q

Na+-K+ ATPase

A

cytoplasmic Na+ binds
pump ATP-phosphorylated
conformation change (Na+ release)
extracel K+ binds (dephosphorylation)
pump returns to conformation (K+ release)

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4
Q

Na+-K+ ATPase ratio in and out

A

3 Na+ out
2 K+ in

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5
Q

experimental methods for ion channel investigation

A

patch-clamp electrophysiology (measure V change across PM)
(cryo) electron microscopy
X-ray crystallography

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6
Q

Vm

A

Vi-Vo

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7
Q

equilibrium potential

A

when ion flux in/out is balanced

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8
Q

Nernst equation

A

E ion= zF/RT ln( [ion] inside/[ion] outside)
simplified to > 61/z (log([ion]out/[ion]in)

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9
Q

shaker potassium channel

A

KCNQ1
Sh gene in drosophilia
a/b sub units
shorter lifespan and less sleep efficiency

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10
Q

closest human homologue of drosophilia Sh gene

A

KCNA3

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11
Q

gating types

A

ligand
voltage
mechanical

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12
Q

TTX

A

tetrodotoxin
blocks Na channels

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13
Q

ion channel structure investigation

A

amino acid structure> side chains predict structure
hydrophobic = transmembrane
hydrophilic = extramembrane

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14
Q

X-ray crystallography

A

crystallize, X-ray > e- density map > atomic model

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15
Q

positives of X-ray crystallography

A

any size molecule/ macromolecule

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16
Q

negatives of X-ray crystallography

A

may damage protein
may take years

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17
Q

cryo-electron microscopy

A

frozen in any state and microscopy

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18
Q

positives of cryo-electron microscopy

A

any size/ macro
near-atomic resolution
fastc

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19
Q

nuclear magnetic resonance

A

dissolved and radioactively labelled

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20
Q

negatives of nuclear magnetic resonance

A

larger molecules can’t be conserved

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21
Q

characteristics of ion channels difficult to crystallize

A

transmembrane
large
multi[ple conformations/ sub-units
dynamic and disordered
low solubility

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22
Q

alpha fold

A

future structure prediction of protein via databanks
:) rapid

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23
Q

no. homologue domains in K channel

A

4

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24
Q

Na+ trajectory/ elution

A

tortuous trajectory
slow elution

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25
Q

K+ trajectory/ elution

A

straight trajectory
fast passage

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26
Q

K channel selectivity filter

A

narrow selectivity filter
mutations can abolish selectivity

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27
Q

N-type channel inactivation

A

amino acid N-terminus occlude intracellular side of pore
rapid inactivation

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28
Q

C-type channel inactivation

A

hinged lid
conformational change at selectivity filter/ extracel entrance
slow inactivation

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29
Q

PETAFLOP

A

measurement unit for 10^16 complex operations per second

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30
Q

major extracellular ions

A

cations: K/Mg
anions: phosphate/ amino acids

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31
Q

major intracellular ions

A

cations: Ca/ Na
anions: Cl

32
Q

RMP

A

-70mV
maintained via K+ leak channels and ATPase pumps

33
Q

Action potential

A

rid change in RMP
sudden reverse in membrane polarity

34
Q

stages of action potential

A

resting
depolarisation (-70> +30 mV)
repolarisation
hyperpolarisation

35
Q

v-gated channels

A

Na+ enters
K+ leaves

36
Q

Na+ gate threshold

A

-55mV
fast opening v-gated
automatic/ fast v-gated
slow/ automatic inactivation from closed

37
Q

K+ gate closure

A

slow opening/ closure

38
Q

absolute refractory period

A

no AP generated
Na+ channel inactivated

39
Q

relative refractory period

A

AP generation w large stimulus
Na+ channels recovered
K+ channels still open

40
Q

nociception

A

sensory nervous system’s process of encoding potentially harmful stimuli.
Mediated by ion channels

41
Q

stimuli transduction

A

through nociceptors, transmitted up primary afferent nociceptor, modulated through interneurone, up spinothalamic tract into thalamus via thalamocortical projections then brain perception

42
Q

nociceptor fibre types

A

A beta
A delta
C fibre

43
Q

what do a beta fibres detect?

A

non-noxious mechanical stimuli

44
Q

what do a delta fibres detect?

A

noxious mechanical stimuli

45
Q

what do C fibres detect?

A

noxious heat and chemical stimuli

46
Q

myelination of nociceptive fibres

A

a beta myelinated
a delta lightly myelinated
c is not myelinated

47
Q

diameter of nociceptive fibres

A

a beta large
a delta medium
c is small

48
Q

function of nociceptive fibres

A

a beta is proprioception
a delta is nociception
c is nociception

49
Q

thermal threshold of nociceptive fibres

A

a beta has no thermal threshold
a delta is ~53 (type I) /47 C (type II)
c is ~43 C

50
Q

transient receptor potential channels

A

ion channels responding to heat/acid/reactive chemicals/ enviro cold/ cold hyperalgesia
additive effects

51
Q

acute vs chronic pain

A

acute <3 months
chronic > 3 months

52
Q

pain classes

A

normal
inflammatory
neuropathic

53
Q

somatic pain

A

peripheral nervous system
specific localisation
a delta and c fibres
pain-relief response

54
Q

visceral pain

A

viscera (uterus/ intestine/ kidneys/ stomach)
non-specific region
a delta and c fibres
autonomic symptoms
poor pain relief response

55
Q

inflammatory pain

A

macrophage/ mast cell/ neutrophil/ granulocyte regulated
treatment> COX2 inhibition
localized pain and swelling
persistent/ chronic nature

56
Q

neuropathy

A

damage causing changes to expression/ post-trans mod of nociceptors
not easily repaired
v specialized
opioid/ anticonvulsants/ Na+ channel blocker/ NMDA antagonist

57
Q

pain relief targets

A

nociceptors
NaV channels

58
Q

pain relief issues w nociceptors

A

heterogeneous pain response
>1 nociceptor
redundancy
side effects
other tissue expression
BBB non-permeable to drugs

59
Q

NaV channel target

A

alpha sub-unit at VGSC
at dorsal root ganglia
enrichment or exclusive depression

60
Q

lidocaine

A

reversible binding to inner pore of V-gated Na+ channels in open/ inactivated states
greater affin for inactivated channels (not resting)
non-selective

61
Q

cystic fibrosis

A

mutation to CFTR gene
Cl- influx dysfunction
mucus accumulation and inflammation
genetic linkage
monogenic/ autosomal recessive
100% penetrance

62
Q

class I CF mutation

A

no CFTR from mRNA

63
Q

class II CF mutation

A

protein folding and trafficking failure

64
Q

class III mutation

A

gating failure

65
Q

class IV mutation

A

decreased stability at membrane

66
Q

class V mutation

A

insufficient CFTR quantities

67
Q

linkage mappong

A

mendelian inheritance pattern of single gene trait
segregated trait in fam
map SNP to locus

68
Q

SCN9A gene voltage gate

A

1.7 NaV
expressed by dorsal root ganglia sensory neurone
contributes to rising phase
amplifies subthreshold stimuli
TTX responsive
fast kinetics

69
Q

paroxysmal extreme pain disorder

A

autosomal dominant
severe pain in rectal/ ocular/ mandible
chewing/ heat triggers
childhood onset
impaired inactivation

70
Q

inherited erythromelalgia

A

autosomal dominant
burning pain in hands and feet
exercise/ heat triggers
childhood onset
enhanced activation

71
Q

small fibre neuropathy

A

loss of function
autosomal dominant

72
Q

inherited erythromelalgia mutation

A

L858H mutation in 2nd domain
lowers activation threshold therefore NaV1.7 open more readily to smaller depolarizations prolonged channel opening due to slow inactivation
^ramp response
shift v-dependence of in/activation for ^hyperpolarized potential inactivation

73
Q

PEDP mutation

A

decreases channel activation threshold
delayed channel inactivation
^ response to repetitive stimulation

74
Q

CIP

A

complete insensitivity to pain

75
Q

complete insensitivity to pain

A

autosomal recessive
complete sensation loss
non-sense mutations in domains 1/11
premature stop codon > truncated protein

76
Q

therapies for complete insensitivity to pain

A

small molecules mimicking toxin binding (belter PK/PD)
botox *doesn’t target NaV

BMS2002 (5 decks)

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