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Neuroscience and Mental Health > Pain I > Flashcards

Pain I Flashcards

1
Q

Types of pain?

A
  • somatic (cutaneous-sharp or deep tissues-dull)
  • visceral (organ tissue-dull in thorax/abdo/pelvis)
  • neuropathic (nerve lesions, not receptors)
  • migraine
  • phantom (in absent limb)
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2
Q

Difference between nociception and pain

A

Nociception: sensing damage

Pain: experience for brain

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3
Q

Acute pain vs Chronic pain?

A

Acute: sudden, self-limiting]- < 6 months

Chronic: sudden or gradual, remission/exacerbation ]- >6 months

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4
Q

Sensory neurons involved in pain and relative diameters?

A
  • Aβ fibres: large diameter (>50μm)
  • aδ fibres: medium diameter (25-50μm)
  • C-fibres: small diameter (20-25 μm)
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5
Q

Difference between Aβ, aδ, and C-fibres (not diameter)?

A
  • Aβ fibres: heavily myelinated (touch, not pain)
  • aδ fibres: thinly myelinated (acute pain)
  • C-fibres: unmyelinated (chronic pain)
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6
Q

Areas of the brain that are involved in pain?

A
  • SI: primary sensory cortex
  • SII: secondary sensory cortex
  • anterior insula
  • cingulate gyrus
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7
Q

Specificity Theory of Pain (Descartes)?

A

Intensity of pain is directly related to amount of associated injury

NB: DOES NOT APPLY FOR CHRONIC PAIN

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8
Q

Gate Control Theory of Pain (Ronald Melzack, Patrick Wall)?

A

Gates open: pain messages get through more easily -> maybe intense pain

Gate closed: pain messages are prevented from reaching brain -> might not be experienced at all

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9
Q

Chemical factors that mediate pain?

A
  • Bradykinin
  • Prostanoids
  • Nerve Growth Factor (NGF)
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10
Q

Activation mechanism of bradykinin for pain?

A

Binds to receptor (GPCR) -> PLA2 activation -> converts arachidonic acid to prostanoids

AND PLC -> PKC

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11
Q

Activation mechanism of prostanoids (PGE2) in pain?

A

-> nociceptive neurons release COX -> arachidonic acid (AA) -via COX-> AA synthesises PGE2

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12
Q

What triggers prostanoid activation?

A
  • pain
  • immune cells (in response to inflammation)
  • pro-inflammatory cytokines (TNF-a)]- induces COX-2
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13
Q

Aspirin effect on prostanoids?

A

Blocks COX -> reduced PGE2

[painkiller]

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14
Q

Mechanism of NGF in pain?

A

NGF binds to TrkA -> increased peripheral sensitivity of nociceptive neurons AND increased Na+ channels

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15
Q

Clinical effect of NGF antibody?

A

Painkiller

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16
Q

Where is TrkA expressed?

A

Selectively expressed on unmyelinated nociceptive sensory neurons (C-fibres)

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17
Q

Neurotransmitters for pain and their receptors?

A
  • Glutamate (AMPA, NMDA)]- excitatory

- GABA (GABA-A, GABA-B)]- inhibitory

18
Q

Glutamate’s role in pain pathway?

A

Tissue damage -> sensory neuron releases glutamate -> post synaptic Na+ influx -> AP -> pain signal to CNS

19
Q

Effect of GABA on pain pathway?

A

If too much pain -> brain central descending inhibitory pathway releases GABA -> Cl- influx -> hyperpolarisation -> decreased AP

20
Q

Effect of NMDA receptor stimulation on pain pathway?

A
  • c-fos production
  • prostanoid production
  • nitric oxide production
21
Q

Channels involved in pain pathways?

A
  • TRP channels
  • ATP-gated channels
  • Ca2+ channels
  • Na+ channels
22
Q

Structure of TRP channels?

A

[only expressed by nociceptive sensory neurons]

non-selective cation channel (Na+/Ca2+)

Gated by capsaicin, anandamide, increase temperature, decrease pH

23
Q

TRP KO -> ?

TRPV1 antagonists -> ?

A

TRP KO -> impaired detection to painful heat stimuli

TRPV1 antagonists -> block pain (but temp fluctuates)

24
Q

Why are ATP-gated channels important?

A

ATP not normally in the extracellular domain i.e. it’s a marker of tissue damage/cell death

25
Q

Types of ATP-gated channel?

A
  • P2X (3,4)]- ligand gated ionotropic

- P2Y (G-protein coupled)

26
Q

What is P2X-3

A

Non-selective cation channel (Na+, Ca2+)

27
Q

What is tactile alloydynia?

A

Increased sensitivity so even light touch can cause pain

28
Q

Mechanism of tactile alloydynia

A

?-> ATP release-> P2X4 on microglia -> more BDNF -> reduced KCC2 (Cl efflux pump) -> increase intracel Cl

GABA release -> Cl- moves down conc gradient -> intracel Cl > extracel Cl -> depolarisation -> pain (AP) -> [brain senses more pain] -> more GABA release -> cycle continues

NB: GABA-r is open but retrograde Cl flow due to conc gradient

29
Q

Structure of Ca2+ channels in pain?

A

4 subunits (α1, β, γ, α2δ)

ion-selective filter EEEE

α1 chaperones α2δ to membrane (blocked by CCB)

4th transmembrane domain is +ve (voltage sensor)

30
Q

Structure of Na+ channel in pain?

A

9 α-subunits]- Nav1.7, 1.8, 1.9 are involved in pain

Ion-selective filter: D+E+K-A pore loops hang off within pore

Inactivation gate (IFN) tripeptide can black Na) entry

Voltage sensor: every 3rd position of the 4th trans-membrane segment has +ve charge

31
Q

Outcome of point mutation of DEKA-> DEEA

A

[DEKA is ion-selective filter on Na+ channel]

DEEA is Ca2+ permeable -> not viable

32
Q

Outcome of tetrodotoxin (TTX) from Fugu fish?

A

Blocks Na+ (except 1.5.,1.8,1.9)

Resp failure (heart and pain unaffected)

[NB: serine in Nav1.8 confers resistance to TTX]

33
Q

Location and properties of Nav1.7?

A
  • found at sensory nerve endings
  • quick to open, quick to close
  • long refractory period
34
Q

Outcomes of Nav1.7 mutation?

A
  • unable to feel pain
  • paroxysmal extreme pain disorder (gain of function, constant Na+ in pain signal)
  • inherited erythromelalgia (gain of function, L858H mutation -> prolonged opening)
35
Q

Location and properties of Nav1.8?

A

NB: key subtype in pain pathway

  • located at axons, exclusively at C-fibres
  • slower to close
  • minimal refractory period
36
Q

PGE2/bradykinin effect on Nav1.8?

A

Enhances TTX resistance Na+ current (lower threshold)

37
Q

Outcome of Nav1.8 KO?

A

Don’t feel pain

38
Q

Gain of function mutation of Nav1.8 -> ?

A

Gain of function mutation -> painful neuropathy

39
Q

Overview of Nav1.9?

A
  • Leaky, persistent current

- Sets RMP

40
Q

Nav1.9 KO -> ?

A

Nav1.9 KO -> normal response to mechanical and thermal stimuli

Neuroscience and Mental Health (65 decks)

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