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Medneuro - M2-3 - Neuronal systems > Somatosensory pain- Lewin > Flashcards

Somatosensory pain- Lewin Flashcards

1
Q

what are the 2 main sensations of the somatosensory system? what are the main receptor types?

A
  1. touch - mechanoreceptors

2. pain/nociception- nociceptors

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2
Q

somatosensory cells…

a. mechanoreceptors have small cell body and are lightly to not myelinated and nociceptors are myelinated with large cell body
b. nociceptors have small cell body and are lightly to not myelinated and mechanoreceptors have large cell body and long axons
c. both nociceptors and mechanoreceptors have the same developmental origin
d. the axon of nociceptors has a large diameter because they need to transmit signal over very long distances

A

b

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3
Q

what types of somatosensory fibres are there?

A
  • A-alpha and ß fibres- myelinated, fast signal transduction, can be nociceptors and mechanoreceptors. these nociceptors deliver the 1st pain (spike very shortly after painful stimulus)
  • A-gamma fibres - all nociceptors, thinly myelinated, small to medium diameter, responsible for mechanical, chemical, thermal sensation; deliver the ‘2nd pain’ which comes later after stimulus.
  • C fibres- the vast majority of nociceptors, unmyelinated fibres with very small diameter. these fibres are activated much later and are responsible for long lasting 2nd pain
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4
Q

types of mechanoreceptors?

A
  • slow adapting mechanoreceptors (SA) - 50% of mechanoreceptors, respond to static phase of nociception
  • rapidly adapting (RA)- respond during the movement phase of stimulus
  • D-hair- dawn of animals (but we have that too); the most sensitive mechanoreceptors
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5
Q

types of nociceptors?

A
  • Amechanic nociceptors (AM)- pricking pain, respond to static phase of stimulus ‘ electric fence’ (~12%)
  • C-fibres-mechano-heat-nociceptors - respond to heat and temperature changes (spike starts when kin reaches temp of 43-45º); polymodal response to 2 different types of stimuli and some respond to cold temps. (~40%)
  • C-fibres-mechanociceptors- respond only to mechanical stimuli.
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6
Q

sensory mechanotransduction…

a. is slow (takes seconds to reach peak)
b. is extremely fast and sensitive (in the nm range)
c. can be fast or slow, depending on the type of fibre
d. is dependent on TrkB receptors

A

b

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7
Q

mechanical stimuli…(which statement is WRONG?)

a. initiate the opening of a channel (depending on stimulus intensity)
b. follow transduction–>spike initiation–>propagation
c. generate a second messenger response

A

c

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8
Q

characteristics of slowly adapting mechanoreceptors (SAM)

A
  • 55% of all Aß fibres innervating the skin and ~12% of all DRG neurons innervating the skin
  • sensation of touch, skin indentation and slip
  • response (and AP) persist and remains constant from the start of the stimulus
  • neurons responding only to movement, not to amplitude (intensity)
  • 2 types: I- innervate merkel cells; II- respond to ruffini corpuscles
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9
Q

characteristics of rapidly adapting mechanoreceptors (RAM)

A
  • 45% of all Aß fibres innervating the skin and ~10% of all DRG neurons innervating the skin
  • sensation of touch, skin indentation and slip
  • response rapidly changes, firing does not respond to movement
  • response is a mix between skin indentation and velocity (unlike SAM)
  • 2 types: I- Meisner’s corpuscles; II- Puccini corpuscles
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10
Q

what is the advantage of the spider slit preparation in the study of mechanoreceptors?

A

one can stimulate the receptor ending and record both the receptor AP and receptor current, because the organ has a distinct morphology, with the slit at the end and the cilium at the joint.

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11
Q

why has the study of mechanoreceptors in C.elegans contributed to the study of sensation?

A
  • the organism is very simple and yet still has nociceptors and mechanoreceptors
  • there is similar transduction currents in both C.elegans and mammals (highly conserved mechanism)
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12
Q

mechanosensitive neurons in C.elegans… (which answer is WRONG?)

a. each neuron is sufficient to show behaviour
b. has 15 genes which code for mechanosensitive neurons
c. all genes code for ion channels and are necessary for response
d. only 2 out of 15 genes code for mechanosensitive ion channels and the rest code for domains and membrane proteins
e. the channels on their own are not mechanosensitive but when combined with other genes/domains they become mechanosensitive

A

c

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13
Q

deletion of Mec4 and 10 in C.elegans….

a. abolishes transduction (loss of mechanosensitive current)
b. decreases mechanosensation but does not abolishes it
c. is important for touch –> loss of tactile sensation
d. does not change response to mechanical stimulus

A

a

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14
Q

STOML3 KO mice…

a. died
b. survived but were not sensitive to mechanical stimuli
c. had increased mechanosensation
d. did not change mechanosensation

A

b

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15
Q

the morphology of Piezo2?

A
  • located at terminal endings of mechanoreceptors
  • fast mechanotransduction
  • located at hail follicles: hair moves–> pushes nerve ending –> channel activation
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16
Q

deletion of Piezo2…(which statement is wrong?)

a. abolishes mechanosensitivity of Aß mechanoreceptors
b. can only work as a conditional KO
c. can be done in embryonic cells
d. only required for mechanical response of Aß fibres (not in nociceptors)
e. preserves pain reaction but decreases dynamic response

A

c

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17
Q

How come does deletion of Piezo2 not changes nociceptive response, if both Piezo2 AND C-fibres use RAM to generate their response?

A

Piezo2 makes rapidly adapting mechanoreceptors (RAM) which is why its deletion abolishes mechanosensitivity of Aß mechanoreceptors. C-fibres, indeed have rapidly adapting response too, however, they potentially have other channels other than Piezo to preserve pain reaction.

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18
Q

STOML3…

a. increases the response of Piezo2 to increase touch sensitivity
b. is enhanced by Piezo2 to increase touch sensitivity
c. is down-regulated by Piezo2 to increase sensitivity of Piezo2
d. inhibits the activity of Piezo2 shortly after presentation of mechanical stimulus
e. depends on Mec2 activity

A

a

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19
Q

patients who don’t have touch sensation…

a. don’t have STOML3
b. don’t have Piezo2
c. don’t have Mec4 and 10
d. have hyperactive STOML3 channels

A

b

20
Q

describe the microneurographic technique. What are the advantages of the method?

A
  • first invented in 1965
  • a single tungsten metal electrode is inserted to contact a single afferent fibre
  • the electrode is connected to an amplifier to record the activity of a single fibre

advantages:
- one can record from a single receptor and this map out the characteristics of different receptor types.

21
Q

type I SA…(which of the following statements is/are correct?)

a. respond to Merkel cells
b. have vey large receptive fields
c. have very small receptive fields
d. change dramatically across species
e. are edge sensitive and are most dense in the fingertips

A

a, c, e

22
Q

type I RA…(which of the following statements is/are correct?)

a. respond to Merkel cells
b. respond to Meisner’s corpuscles
c. have very small receptive fields
d. highly conserved across species
e. are edge sensitive and are most dense in the fingertips

A

b, c, d, e

23
Q

type II SA…(which of the following statements is/are correct?)

a. respond to Merkel cells
b. respond to Ruffini’s corpuscles
c. respond to skin stretching
d. have a small innervating density each corpuscle is innervated by a single axon
e. are edge sensitive and are most dense in the fingertips

A

b, c, d

24
Q

type II RA…(which of the following statements is/are correct?)

a. respond to Puccini corpuscles
b. respond to Ruffini’s corpuscles
c. respond to skin stretching
d. have large and obscure borders
e. are very sensitive

A

a, d, e

25
Q

The microneurographic technique was modified in Sweden, so instead of recording from the axon, they stimulated the different fibres, and asked subjects to report their sensation. their finding were…

a. RA I induced feeling of localised vibration; SA I - feeling of pressure; RA II - non localised vibration; SA II- no sensation at all
b. RA I induced feeling of pressure; SA I - feeling of localised vibration; RA II - no sensation at all; SA II- non localised vibration
c. SA I induced feeling of pressure; RA I - no sensation at all ; RA II - non localised vibration; SA II- feeling of localised vibration
d. a. RA I induced feeling of non localised vibration; SA I - feeling of pressure; RA II - localised vibration; SA II- no sensation at all

A

a

26
Q

why did they use a ramp & hold stimulation in touch studies?

A

because the ramp is the stimulus intensity over time and the neuron responds to the frequency as mechanosensation is about vibration. –> rough objects will have a higher frequency than smooth objects.
–> increasing the frequency vibration gives lower lever of skin indentation and vice versa

27
Q

describe the organisation of fibres in the spinal cord

A
  • the spinal cord is somatotopically organised.
  • the synapses in the spinal cord are organised and branched in a columnar fashion.
  • the synapses in the spinal cord originate from specific collaterals (e.g. the medial collaterals give rise to afferents that produce the receptive fields…)
  • each receptor type has a specifically mapped spatial organisation
  • sensitivity of the receptor is dependent on the height of the afferent.
28
Q

which 2 pathways carry out somatosensory information to the brain?

A
  1. DRG/dorso-caudal lemniscal system: carries out information only from mechanoreceptors (no nociceptors).
  2. anterolateral pathway- information from both mechanoreceptors and nociceptors
29
Q

what is the difference between sub modality segregation and sub modality convergence?

A
  1. sub-modality segregation:
    each mechanoreceptor is responsible for different information type (texture, shape, motion…). according to this model:
    - SA1 cells deliver information about texture and shape
    - RA cells deliver information about grip control and motion
    - PC deliver information about vibration
  2. sub modality convergence:
    each receptor type contributes to each of the aspects of sensation on different levels:
    - PC are most sensitive to vibration and grip control because they sense the smallest change in stimulus.
    - shape of objects and motion is mostly sensed by SA1 and RA.
30
Q

what is the transduction velocity of C fibres?

A

1 sec

31
Q

which pathway relays information about pain?

A

anterolateral pathway

32
Q

why is it harder to conduct pain studied in humans?

a. nociceptors are less sensitive to a single stimulus
b. nociceptors are much slower
c. hard to recruit subjects because they don’t want to feel pain
d. all of the above

A

c

33
Q

what do we know about signal transduction through C fibres and A-gamma fibres from primate and human studies?

A
  • C- fibres - judgement of pain is stronger in the first 2 seconds of pain
  • A-gamma fibres- sensation is consistent overtime, due to summation of AP from multiple fibres at a time, in order to build a pain threshold.
  • Studies:
    1. nociceptor response to force stim. (monkeys): in A fibres, more fibres have to be activated together in order to perceive pain (spatial summation), which linearly correlate with force level;

–> compared w. human pain rating studies: subjects reported pain before and during block of A fibres: before the block pain rating was much higher in respoinse to force. –> A-gamma fibres predominantly control pain threshold

34
Q

what is happening in hyperalgesia?

A

Hyperalgesia is the effect of tissue injury on pain sensitisation. A stimulus that would normally produce a very mild to no pain response, produces a much stronger pain response very rapidly, because the tissue is very sensitive.

35
Q

why does injury produce hyperalgesia?

A
  1. inflammatory soup- tissue damage activates many immune factors and cellular organelles release many chemical factors (ATP, glucose…) into the extracellular space in order to signal the immune system abut the damage. also macrophages release factors that activate proteins, and acidifying factors–> tissue more sensitive to stimuli
  2. nociceptors are also chemo-receptors that cn sense changes in the cell and its environment –> respond to these changes
36
Q

how can you test tissue sensitisation experimentally?

A
  1. before injection- stimulate tissue (5 bar) –> no response
  2. inject ‘inflammatory soup’
  3. some time after injection–> stimulate the same as before (5 bar) –> tissue responds much faster to the same stimulus
37
Q

what is the difference between hyperalgesia and sensitisation?

A
  • hyperalgesia- subject response to stimulus –> decreased pain threshold
  • sensitisation- fibre response to stimulus–> decreased threshold for response.
38
Q

heat-hyperalgesia…

a. is completely peripheral
b. depends on TRPV1
c. only occurs when skin temperature exceeds 43º
d. occurs after thalamic lesions

A

a

39
Q

TRP channels….

a. TRPV1 is very common and responds to heat (>43º) and toxins such as capsaicin
b. are differently distributed and respond to different temperature ranges
c. TRPM2 responds to temps > 52º
d. require activation of many different kinds in order to generate a response to a specific temp.
e. all of the above

A

e

40
Q

describe the axon reflex response

A

in axon reflex response, the stimulus doesn’t need to be processed in the CNS, but elicits a strong peripheral response. the stimulus can travel not only along the axon, but flares out also to its branches.
Axon is activated–>activating C-fibres –> C-fibres release peptides –> produce peripheral flare response

41
Q

what happens to the tissue after a heat injury

A

heat injury –> flare response in the tissue damage are –> tissue is much more sensitive in the area of the flare

42
Q

what is the difference between heat-hyperalgesia and mechanical hyperalgesia?

A

in mechanical hyperalgesia, the response isn’t limited to the flare borders so the response isn’t resptricted to the injured axons

43
Q

NGF hyperalgesia…

a. adult mice develop heat hyperalgesia and mechanical hyperalgesia after injection of NGF which lasts several days
b. adult mice develop heat hyperalgesia and mechanical hyperalgesia after injection of NGF which permanent
c. heat hyperalgesia develops after mechanical hyperalgesia after injection of NGF
d. NGF cures hyperalgesia
e. infant mice develop heat hyperalgesia and mechanical hyperalgesia after injection of NGF which lasts several days

A

a

44
Q

NGF hyperalgesia…(which answer is WRONG?)

a. induction of heat- and mechanical hyperalgesia after injection of NGF
b. can be treated with TrkB to prevent sensitisation if the tissue
c. can be treated with TrkA to prevent sensitisation if the tissue
d. NGF injection leads to release of BDNF which increases amounts of TrkB and NMDA receptors and causes central sensitisation

A

b

45
Q

what are the causes for neuropathic pain?

A
  • diabetes
  • HIV
  • Herpes zoster
  • toxins/channelopathy
  • trauma
46
Q

in neuropathic pain…(which answer is WRONG?)

a. activation of nociceptors which have been detected from their target but are still mechanosensitive
b. can be treated by blocking mechanoreceptor
c. can be treated by deactivation of STOML3
d. can be treated by blocking Piezo2
e. has been studied through CCI models

A

d

Medneuro - M2-3 - Neuronal systems (6 decks)

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