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Neuro_week3 > Nociception-pain-temp > Flashcards

Nociception-pain-temp Flashcards

1
Q

Structure of pain and temp axon

A

bifurcates with one receptor branch and central axon that enters CNS

both detected by sensory endings

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2
Q

structure of sensory ending receptor for pain and temp axon

A

free nerve endings (but not pacinian, merkel, etc.)

afferent fibers have cell body in DRG and central axon enters cord

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3
Q

pathway of pain and temp

A

1) sense in primary neuron
2) dorsal horn synapse
3) 2nd order neuron decussates at anterior commissure and ascend in spinothalamic tract
4) synapse on 3rd orde rneuron in VPL thalamus
5) project to somatosensory cortex or 2nd order neuron can also go to hypothal

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4
Q

know receptors that detect temp info

2 types of temp receptors on sensory endings

which are there more of

A

1) warm receptor (30-48 degr C)
= C fibers

2) cold receptors (10-37 degrC) = Adelta fibers

MORE COOL RECEPOTRS

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5
Q

know how temp receptors encode info

more sensitive to absolute temp or rate of change?

A

warm and cold receptors alter firing freq of AP in response to change in temp

more sensitive to rate of change than absolute temp

ex = cold receptor fire at steady rate then burst of rapid firing as temp dropping then slow again

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6
Q

in response to painful stim what are two types of pain? what are they separated by?

A

separated by time

1st pain = pricking pain (local and well tolerated, carry by Adelta fibers (slight myelin)

2nd pain = aching, burning pain; smaller, unmyelinated C fibers; poor localize and poor tolerate

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7
Q

which is better localized pricking or burning sensation

A

pinprick because Adelta fibers have smaller recepitve fields so better spatial discrim

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8
Q

2 major blocking manipulations
pressure

what does this cause?
what happens with incr pressure

A

1) pressure induces anoxia (first fibers affected are metab active = Aalpha and Abeta fibers

causes loss of touch, vibration, propioception, joint movement WITHOUT PAIN
but as pressure incr, pain fibers also affected (Adelta before C) and only sense burning

as even more pressure, C fiber block and no sensory

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9
Q

2 major blocking manipulations
local anesthetics

effect of 3 diff doses (low, med, high)

A

block small diameter fibers at concentration –> suppress burning pain first

higher doses block pricking pain

highest dose block touch and motor

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10
Q

example of activating manipulations?

what happens if incr intensity

A

electrical stim
single, low intesnity stim can activ Aalpha and Abeta fibers –> sensation of touch and join movement without pain

higher intensity = pricking pain

higher and repetitive = burning pain

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11
Q

what are afferent fibers for polymodal pain receptors

A

C fibers as afferents

have different receptors on different segments of the ending

also have diff receptors on single ending and respond to variety of stim

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12
Q

VR1 receptor activated by?

where is it located?

A

activ by capsaicin but also weakly responds to acid and moderate heat (43 degrC)

found in vanilloid moiety containing compounds and on polymodal nociceptors

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13
Q

ASICs respond to?

P2X responds to?

A

ASICs = acid

P2X = purines (ATP)

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14
Q

chemicals that act as pain activators

define
examples

A

activators = depol nerve ending to threshold

ex = bradykinin, K+, acid, serotonin

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15
Q

chemicals that act as pain sensitizers

define
examples

A

depolarizes but not to threshold and easier for activators

ex = prostaglandins, substance P, ATP, acetylcholine, serotonin

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16
Q

what type of pain info is carried by C fiber affernts

A

2nd pain = burning/aching poorly localized pain that is not well tolerated

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17
Q

location of first synapse in pain pathway

what NT operate here?

A

in dorsal horn of spinal column in the substantia gelatinosa = Rexed’s lamina II

major excitatory NT = glutamate

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18
Q

2nd order neurons in dorsal horn of pain pathway have what receptors

A

2 receptors = AMPA and NMDA
both ionotropic

AMPA = rapid synaptic response
NMDA = simultaneous depol + glutamate

so fast and slow response

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19
Q

Difference btwn AMPA and NMDA at dorsal horn synapse

A

AMPA = rapid synaptic response

NMDA = slow excitatory potential

AMPA = require only glutamate

NMDA = require glutamate + depol to kick out Mg2+ +

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20
Q

what does NMDA recepotr gate?

produces __ changes in excitatability

A

gates Ca2+ channel so incr Ca2+ influx

produces long lasting changes in excitability

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21
Q

phosphorylation of NMDA by ___ does what?

A

phosphorylation by PKC and tyrosine kinase removes requirement of depol and NMDA can’t bind Mg2+

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22
Q

prolonged release of glutamate at dorsal horn enables NMDA to what?

A

more easily propagate AP –> central sensitization

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23
Q

NT at dorsal horn synapse
Glutamate released by?
acts on?

A

released by primary nociceptive sensory neurons at first synapse

acts on postsyn NMDA and AMPA

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24
Q

NT at dorsal horn synapse
Substance P
how is it released?

what does it bind on? and effect?

A

intense stim of C fibers releases at presynap terminal

binds on NK1 receptor and causes closing of K+ channels and depol

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25
Q

overall effect of substance P

A

enhancement and prolong actions of glutamate

may diffuse to many dorsal horn neurons for broad central sensitization at dorsal horn for long time

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26
Q

basis for peripheral sensitization

what is sensitization of nocicpetors also known as?

A

aka primary hyperalgesia because incr sensitivity to pain occurs at first site in path

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27
Q

agents that sensitize nociceptors

A

1) prostaglandins
2) substance P
3) ATP
4) ACh
5) serotonin

these decr threshold for activation of nociceptors

28
Q

why do sensitizing agents decr threshold for activation of nociceptors

A

when you injure yourself, you stim C pain fibers

–> causes release of substance P

–> sensitize nociceptors in area bigger than original wound

therefold, a smaller stim needed to activate them promoting changes for better repair

29
Q

basis for central sensitization

wind-up phase

A

1) as C fibers stim, postsyn AMPA receptors stim first since only glutamate around
2) if stim persistent, both glutamate + postsyn depol activ NMDA (larger response)
3) causes wind-up = stim dependent enhancement of postsyn response of dorsal horn neuron

30
Q

basis for central sensitization

NMDA receptor phosphorylation

A

1) incr in intracellular Ca2+
2) causes phosphorylation of NMDA by PKC and tyrosine kinase inhibiting Mg2+ binding to NMDA
3) NMDA no longer requires depol so easier open
4) P-NMDA and AMPA now both open by glutamate alone

31
Q

basis for central sensitization

effect of substance P

A

not removed by reuptake so persists

and can diffuse to many dorsal horn neurons –> broad sensitization

32
Q

basis for analgesic action of aspirin

A

ASA inhib cyclooxygenase that converts arachidonic acid to prostaglandin

by block synth of prostaglandin, aspirin prevents nociceptors sensitization (primary hyperalgesia)

33
Q

basis for triple response

A

triple response = central red + wheal + flare

34
Q

central red and wheal

how does it occur?

A

1) tissue damage causes local bradykinin production
2) vasodilates and produce heat and redness (central reddening)
3) incr permeability of capillary membraens –> fluid accum and swelling (edema/wheal)

35
Q

flare

how does it occur?

A

1) bradykinin activ C fiber nociceptors
2) AP propagate toward cell body of DRG and along collaterals to periphery
3) release of substance P surrounding wound site
4) mild vasodilator so pink flare

CALLED “AXON REFLEX”

36
Q

location of action and effects of substance P

where is substance P released?

A

released at synapse and in periphery from C fibers

37
Q

effect of substance P on peripheral collateral

how does it cause flare
how does it sensitize?

A

1) mild vasodilator producing flare in triple response in response to local tissue damage
2) also sensitizes to decr threshold of nocicpetors in tissue damage sites
3) therefore, responses to noxious stim are enhanced –> behavioral changes for better healing

38
Q

effect of substance P in synapse (dorsal horn)

effect of intense stim on C fibers

A

acts as sensitizer

1) intense stim of C fibers terminating in subst gelatinosa causes release of subst P
2) binds NK1 receptors and closes K+ channels –> depol
3) enhances and prolongs glutamate action on AMPA and NMDA –> incr pain sensitization
4) also diffuse to nearby neurons so broad sensitization

39
Q

PAG neurons located where? project where?
the project where?

what NT do they ahve?

A

found in midbrain
project to medulla
then project to dorsal lateral funiculus

medullary neurons are 5-HT

40
Q

effect of 5-HT in spinal cord

use what NT? effect on pain sensation?

A

inhib second order neurons of dorsal horn by exciting inhib interneurons

they use enkephalin and blocks VG ca2+ channels presynap and open K+ channels postsynap

inhib of 2nd order neuron –> decr pain sensation

41
Q

PAG neurons sensitive to?

A

sensitive to opiates

exposing endogenous or exogenous opioids –> greater excitatory output –> greater inhib of 2nd order neurons in dorsal horn

42
Q

stroking or rubbing area of body experinencing pain causes ___

why?

A

decr sensation of pain

because activates non-nociceptive afferent pathways (touch and A-beta fibers)

activates dorsal horn interneurons that inhib synapses activated by nociceptive fibers

43
Q

selective stim of A-beta fibers causes

A

causes reduction of pain (basis of transcutaneous electrical nerve stim)

44
Q

elimination of inputs from A-beta fibers causes

A

incr pain sensation (hyperalgesia)

45
Q

define gate control theory

A

nociceptive inputs open and non-nocicpetive afferents shut gate that leads to central transmission of noxious info

46
Q

basis for placebo effect

PAG receive input from?

ultimate effect?

A

1) PAG receive input from limbic system and cortex
2) but expect to receive pain-releiving drug
3) incr activity in neocortex/limbic
4) PAG activated via secretion of endorphins that stim PAG excitatory output

–> incr stim of inhib interneurons in dorsal horn and inhib of 2nd order neurons in dorsal horn

47
Q

placebo effect blocked by?

A

blocked by naloxone so PAG responsible

48
Q

stress induced analgesia

what does it incr? result?

A

increases limbic system activity

activates PAG and stim of inhib interneurons in dorsal horn

results in inhib of 2nd order neurons in dorsal horn of pain pathway

49
Q

effect of naloxone on stress induced analgesia

A

naloxone blocks some but not all analgesia so stress = opioid + nonopioid mechanism

50
Q

rewiring in neuropathic pain

effect on signals from primary to secondary neurons

A

1) injury causes change in concentrations of neutrophrins
2) promotes inappropriate growth of neurons
3) neurons contact inappropriate targets
4) organization awry
5) primary neurons can’t be organized by stim around appropriate secondary neuron –> wrong signals from primary neurons may stim 2nd neuron

51
Q

role of GABA in neuropathic pain

A

decr GABA + decr GABA and opiate receptors

causes decr inhib signals

decr second order neuron excitation

52
Q

role of microglia in neuropathic pain

causes release of ___

A

after injury, microglia activated (incr ATP attract microglia via purine recepotrs)

release of BDNF
decr expression of KCC2 (extruder of Na)
alters Cl reversal potential
GABA activation causes ecitation

therefore, decr inhib in dorsal horn –> hyperalgesia

53
Q

3 tracts after axons ascend in anterolateral tract

A

1) VPL thalamus
2) reticular formation
3) mesencephalon

54
Q

VPL thalamus = spinothalamic tract contains what info

A

localizes the input (pain and temp)

55
Q

spinoreticular tract cotains what info

A

sends info to hypothalamus, amygdala (behavioral/emotional responses to input) (pain and temp)

56
Q

spinomesencephalic tract contains what info

A

important for descending modulatory influences of pain

57
Q

3 types of pain

A
  1. Nociceptive = acute painful stimulus (flame, overinflated BP cuff, chemicals)
  2. Inflammatory = injury and inflamm signals released
  3. Neuropathic
58
Q

for extreme temperature
extreme temp = Cold = what fibers

extreme temp = warm = what fibers

mechanical are primarily what fiber type

polymodal fibers are all what?

A

cold = C

hot = Adelta

opposite of well being

mechanical = adelta

polymodal = C

59
Q

release of substance P requires

A

repetitive stim of c fibers

60
Q

Distinguish btwn hyperalgesia and allodynia

A

hyperalgesia = incr sensitivity to pain (flare)

allodynia = non-noxious stim like touch becomes painful (sunburn then water in shower hurts rather than feel good)

61
Q

why do you have referred pain

A

a. Due to convergance of inputs from cutaneous and visceral sites but cutaneous ones dominate so therefore have referred pain

62
Q

Tabes dorsalis causes degeneration of ___

what effect

A

Abeta fibers = intolerable pain (losing Abeta because now losing endogenous way to produce analgesia)

63
Q

Electrical stim of back relieves pain how?

A

although fibers ascend and feel pain but also fibers descend and activate enkephalinergic interneuron in many segments

64
Q

Descending modulatory pathway of PAG

A

1) stim PAG
2) project to nucleus raphe magnus = medulla
3) project to dorsal horn of spinal cord (target enkephalinergic inhib interneurons)

65
Q

Types of TTX Receptors

both sensitive to __

A

TTX-sensitive

TTX-resistant = in sensory neurons of heart, CNS

both sensitive to lidocaine

Neuro_week3 (23 decks)

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