Nocioception I & II Flashcards

1
Q

Types of temperature receptors (+fiber types)

A
  • cool receptors (10-37°C)
    • 10x cool vs. warm
    • A(delta)
  • warm receptors (30-48°C)
    • C fibers
  • receptors turn temp info ==> receptor potential ==> action potential
    • frequency of APs indicates intesity
    • can indicate absolute temp and rate of temp change
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2
Q

Anterolateral system tracts

A
  • spinothalamic tract = conveys pain info to thalamus ==> somatosensory cortex
  • spinoreticular tract = conveys pain inputs to forebrain arousal and emotion @ medulla and pons (reticular formation)
  • spinomesencephalic tract = projects to periaqueductal gray region (PAG); desceding control of pain
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3
Q

Anatomical pathway of pain/temp info

A
  • (1°) pain or temp sensory receptor ==> sensory neuron ==> DRG ==> synapse @ dorsal horn
  • (2°) dorsal horn ==> crosses midline @ anterior white commisure ==> ascends @ anterolateral tract ==> synapse @ thalamus
  • (3°) thalamus ==> somatosensory cortex
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4
Q

Pain and temp pathways for head/neck

A
  • trigeminal ganglion neurons ==> enter @ pons ==> spinal trigeminal nucleus
  • spinal trigeminal nucleus = ~ dorsal horn of spinal cord
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5
Q

Types of pain receptors (+ fiber types)

A
  • thermal nociceptors = activated @ extreme temps (<5ºC or >43ºC)
    • hot nociceptors = A(delta) fibers
    • cold nociceptors = C fibers
  • mechanical nociceptors = activated @ intense pressure
    • A(delta) fibers
  • polymodal nociceptors = activated @ high-intensity mechanical or thermal stimuli
    • C fibers
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6
Q

Substance P characteristics

A
  • neuropeptide transmitter @ pain afferents
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7
Q

Vanilloid Receptor characteristics

A
  • class of molecular components on nociceptors
  • VR-1 = capsaicin receptor
    • strongly activated by capsaicin, weakly activated by acids
    • also activated by moderate heat
    • expressed on polymodal receptors
    • activation ==> NSC channel ==> depolarization
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8
Q

Types of pain experienced in response to stimulus

A
  • “first pain” = “pricking” pain
    • tolerable, localized
    • A(delta) fibers
  • “second pain” = burning pain
    • uncomfortable, diffusely localized
    • C fibers
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9
Q

Pain information carried by C fiber afferents

A
  • “second pain”
  • burning pain
  • diffusely localized
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10
Q

Characteristics/examples of pain activators

A
  • compounds can lead to direct activation of nociceptors
  • tissue damage ==> release of cytoplasmic proteases ==> bradykinin
    • activates A(delta) and C fibers
  • potassium
  • acid
    • activates ASICs (Acid-sensing) and VR-1
  • serotonin
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11
Q

Characteristics/examples of pain sensitizers

A
  • agents that reduce the threshold for activation of nociceptors
  • prostaglandins
  • substance P
    • C fibers release during repetitive electrical stimulation
  • ATP, ACh, serotonin
    • can act individually or together as sensitizers
  • activators and sensitizers are likely to be present simultaneosly
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12
Q

Asprin MOA

A
  • Aspirin inhibits enzyme cyclooxygenase (COX)
  • COX normall converts arachidonic acid to prostaglandin
  • Aspirin inhibits prostaglandin formation ==> prevents nociceptor sensitization
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13
Q

Characteristics of the triple response

A
  • reddening, wheal, flare
  • Tissue injury ==> bradykinin
    • ==> vasodilation ==> heat/redness
    • ==> increased capillary permeability ==> edema (wheal)
  • flare = pinkish zone around inflammation
    • C fibers activated by bradykinin ==> APs towards cell body + collaterals and peripheral sites
    • ==> substance P release surrounding wound ==> some vasodilation (less than bradykinin)
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14
Q

Site of first synapse in pain/temp pathway

A
  • various regions of dorsal horn (aka “laminae”)
  • C fiber afferents ==> Rexed lamina II = “substantia gelatinosa”
  • second oder neuron has cell body in substantia gelatinosa
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15
Q

Major NTs and receptors @ first synapse in pain/temp pathway

A
  • Glutamate = major excitatory transmitter
  • AMPA & NMDA receptors
    • both ionotropic
    • AMPA ==> rapid synaptic response
      • glutamate ==> open channel
    • NMDA ==> slower excitatory potential
      • require glutamate + depolarization before channels open
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16
Q

Characteristics of “wind-up”

A
  • “wind-up” = process of central sensitization
  • C fibers stimulate ==> release glutamate ==> activate AMPA receptors first
  • C fiber stimulation = intense + persistent ==> glutamate + post-synaptic depolarization ==> NMDA activated ==> larger post-synaptic response
  • NMDA receptors become phosphorylated ==> removed requirement for depolarization for activation
17
Q

Substance P actions

A
  • intense stimulation of C afferent fibers ==> released both @ periphery and centrally
  • @ periphery ==> some vasodilation
  • @ dorsal horn ==> binds receptor ==> close K+ channels ==> depolarization ==> enhancement and prolongation of actions of glutamate
    • _​_not removed by reuptake ==> persists and diffuses to many dorsal horn neurons ==> broad sensitization
18
Q

Analgesia definition

A
  • inability to feel pain
  • inhibition @ dorsal horn synapse
19
Q

Common method of inducing analgesia

A
  • stimulation of A(beta) fibers ==> activation of dorsal horn interneurons ==> inhibit nociceptive synapses
  • e.g. stroking/rubbing activates touch and A(beta) fibers
  • e.g. transcutaneous electrical nerve stimulation (TENS) ==> stimulate A(beta) fibers @ injured area
    • in contrast: elimination of A(beta) inputs ==> hyperalgesia
20
Q

PAG (periaqueductal gray) region control of pain

A
  • stimulation of PAG @ midbrain ==> powerful analgesic effect
  • PAG neurons ==> medulla ==> medullary neurons use serotonin to excite an inhibitory interneuoron ==> endogenous opiates to reduce pain
    • reason for SSRI use in chronic pain
  • PAG exposure to opiates ==> greater excitatory output from PAG
21
Q

Stress-induced analgesia characteristics

A
  • = adaptive response to stressful conditions
    • e.g. soldiers/athletes unaware of injuries until situation calms
  • stress ==> increased limbic activity ==> activation of PAG
  • involves both opiod and nonopiod-mediated mechanisms
22
Q

Placebo effect characteristics

A
  • administration of inert drug ==> alleviate sx or cures disease
  • belief in drug ==> neocortex/limbic activity increase ==> PAG activation through increased endorphin secretion ==> analgesia
23
Q

Peripheral mechanisms of neuropathic pain

A
  • spontaneous activity in primary sensory neurons ==> stimulus-independent pain conditions
  • TTX-sensitive and TTX-resistant sodium channels contribute to normal and abnormal pain processing
    • nerve damage ==> alteration of distribution/fxn of sodium channels ==> spontaneous discharge
    • ==> tx w/sodium0channel blockers (CNS/cardio SEs)
24
Q

Central mechanisms of neuropathic pain

A
  • nerve injury ==> reduced GABA/opiate receptors ==> decreased inhibition/increased excitability @ dorsal horn neurons
  • nerve injury ==> A(beta) sprout and invade territory of substantia gelatinosa (normally only innervated by C fibers) ==> activated by non-noxious stimuli
  • nerve injury ==> inflammation ==> help develop and maintain neuropathic pain