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Neuro Unit 2 > Pain/temp > Flashcards

Pain/temp Flashcards

1
Q

thermoneutral point

A

33 degrees C; similar firing rates of warm/cool receptors

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2
Q

temp range for cool receptors

A

10-37C

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3
Q

temp range for warm receptors

A

30-48C

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4
Q

temperature range for sensing skin temperature

A

10-48 C

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5
Q

2 classes of temp receptors

A

cool and warm receptors

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6
Q

Are there more cool receptors or warm receptors

A

Cool receptors; about 10x as many warm receptors

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7
Q

where are cell bodies of temperature receptors

A

DRG or trigeminal if in face

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8
Q

where are temp receptors located

A

in the skin on free nerve endings

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9
Q

What type of fibers are cool receptors associated with

A

Aδ

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10
Q

What type of fibers are warm receptors usually associated with

A

C fibers

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11
Q

where is first temperature synapse

A

in dorsal horn of spinal cord and the spinal trigeminal nucleus (for limbs/body, head/neck, respectively)

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12
Q

First order neurons

A

in periphery and synapse on second order neurons in dorsal horn of spinal cord

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13
Q

Where are the second order neurons going

A

Thalamus then to sensory cortex via spinothalamic tract; another tract – spinoreticular tract conveys info via reticular formation to hypothalamus (this info important for control of body temperature – an autonomic function)

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14
Q

spinoreticular tract

A

plays role in emotional response to pain

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15
Q

Tracts of anterolateral system

A

spinothalamic, spinoreticular, spinomesencephalic

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16
Q

Spinothalamic tract

A

conveys pain to thalamus.

  • Projects to nuclei of ventrobasal thalamus (includes VPL, VPM)
  • process info related to localization of pain/project to somatosensory cortex
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17
Q

spinoreticular tract

A

conveys pain inputs leading to forebrain arousal/elicits emotional and behavioral responses via connections to emotional circuits of brain
- terminates in medulla/poins

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18
Q

Spinomesencephalic tract

A

projects to midbrain periaqueductal gray region

- important for descending control of pain

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19
Q

other cortical regions activated in pain processing

A

cingulate gyrus: part of limbic system and contributes to emotional component of pain sensation
insular cortex: processes info related to autonomic component of pain

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20
Q

Where do axons from trigeminal nucleus enter

A

at level of pons– descend to caudal position before forming first synapse

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21
Q

site of first synapse of trigeminal ganglion axons

A

spinal trigeminal nucleus (in region from rostral spinal cord to caudal brain stem)

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22
Q

spinal trigeminal nucleus

A

receives inputs from head/neck via trigemina ganglion neurons

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23
Q

importance of pain

A

warn of probable injury; help avoid or minimize tissue damage

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24
Q

Thermal pain receptors

A

Thermal nociceptors; activated by extreme temperatures (43C)

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25
Q

fibers associated with nociceptors activated by extreme heat

A

Aδ

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26
Q

fibers associated with nociceptors activated by extreme cold

A

C

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27
Q

receptors for Intense pressure

A

mechanical nociceptors– associated with A (delta) fibers

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28
Q

Receptors activated by high-intensity mechanical, chemical or thermal stimuli

A

polymodal nociceptors

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29
Q

fibers associated with polynodal nociceptors

A

C fibers

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30
Q

Vanilloid receptor

A

VR

  • VR-1 = capsaicin receptor
  • strongly activated by capsaicin and weakly by acids; also activated by moderate heat (43C)
  • expressed on polynodal nociceptors
  • receptor part of ion channel complex
  • receptor activated–> non-selective cation channel opens –> depolarization
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31
Q

Other nociceptors

A
  • ion channels gated by ATP/acids
  • ATP opens ionotropic P2X receptors
  • Acid-sensing channels = ASICs (4 different ASIC genes expressed on C fiber nociceptors)
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32
Q

different kinds of pain

A

nocioceptive, inflammatory, neuropathic

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33
Q

Are A (delta) receptors myelinated

A

poor myelination but better than C

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34
Q

Path of 3 anterlateral system

A

Spinothalamic –> thaamus –> somatosensory cortex

Spinoreticular –> reticular formation –> hypothalamus & various thalamic nuclei(behavior/emotion)

Spinomesencephalic –> midbrain –> mesencephaon (descending modulatio of pain)

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35
Q

Anterolateral system sensations

A

pain/temperature

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36
Q

Anterolateral system primary sensory neuron

A

DRG(Aδ, C fibers)

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37
Q

Primary synapse of anterolateral system

A

Dorsal horn (spinal cord)

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38
Q

decussation location of anterolateral system

A

in spinal cord at same level of synapse in dorsal horn

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39
Q

Input vs ascending information of anterolateral system

A

contralateral

40
Q

DCML sensations

A

touch/proprioception

41
Q

Primary sensory neuron of DCML

A

DRG (trigeminal) - A beta

42
Q

1st synapse of DCML

A

Nucleus fasiculus gracilis or cuneatus in medulla

43
Q

Decussation location of DCML pathway

A

medulla

44
Q

Input vs ascending information of DCML pathway

A

Ipsilateral to contralateral

45
Q

when do cool receptors increase firing rate

A

when temperature decreases

46
Q

when do warm receptors increase firing rate

A

when temperature increases

47
Q

transient response

A

tells us about change in temperature per time

48
Q

Sustained response

A

absolute temperature

49
Q

Molecular receptor types

A

ASIC (acid), P2X (inflammation, purigenic receptor–ATP), VR-1 (capsaicin-chemical, temp)

50
Q

type of fibers for pain

A

Aδ and C

51
Q

hyperalgesia

A

increased sensitivity to pain

52
Q

allodynia

A

nonnoxious stimulus now painful

53
Q

Aδ vs C fibers

A
  • both small diameter but C smallest
  • Aδlightly myelinated vs C not
  • both conduct more slowly than A-alpha and beta; Aδ more rapid than C so that information gets to CNS before info from C fibers
  • receptive field associated with Aδ fibers slightly smaller, so Aδ fibers better localized – better spatial discrimination
54
Q

pain sensed by Aδ fibers

A

first pain–localized tolerable pricking pain

55
Q

Second pain

A

sensed by C fibers– burning, intolerbable, diffusely localized, “burning” pain

56
Q

If pressure applied, in what order will you lose sensation

A
  • those in high metabolic demand most vulnerable
  • larger diameter will become nonconductive first
  • lose Aalpha and Abeta (touch/vibration/joint position/joint movement; paralyzed)–>Aδ (prickling pain) –> C (burning pain)
57
Q

Give electrical stimulation, which fibers activated first

A

Aalpha and Abeta (touch/vibration/joint position/joint movement)–>Aδ (prickling pain) –> C (burning pain)

58
Q

give anesthetic, what is suppressed

A

C (burning pain)–>Aδ (prickling pain) –> block motor axons/touch afferents (paralysis)

59
Q

what is released by damaged cells

A

K, ATP, Prostaglandins, acid

- mast cels recruited to tissue damage and release serotonin/other chemicals

60
Q

What compounds are considered activators of nociceptors

A

Bradykinin, acid (H), K, 5HT

- Bradykinin from cleavage from inactive kininogen

61
Q

Sensitizers

A

depolarize neuron a little but not to get full AP; makes it easier for next stimulus to reach AP

62
Q

Examples of Sensitizers

A
  • Prostaglandins, Substance P

- ATP, ACh, 5HT (single or together)

63
Q

Primary hyperalgesia

A

sensitization of nociceptors (since it occurs in first site of pathway)

64
Q

Triple response

A

as a result of injury – characterized by: reddening, wheal and flare

65
Q

In triple response, what is responsible for the redness, edema/ wheal, and flare

A

Flare (pink)- Substance P

Redness and Wheal (edema) - Bradykinin

66
Q

intrathecal

A

within subarachnoid or subdural space

67
Q

Rexed’s lamina II

A

area in substantial gelatinosa of dorsal horn where C fibers terminate

68
Q

Nociceptive afferents synapse

A

dorsal horn of spinal cord (limbs/trunk) or trigeminal spinal nucleus (head/neck)

69
Q

Modality segregation

A

afferents comveying info of different sensory modalities reach CNS in organized manner and segregate to different regions of dorsal horn (laminae)
- Adelta fibers terminate in different laminae

70
Q

referred pain

A

due to convergence of visceral and somatic pain inputs; some pain -activated dorsal horn neurons get input from both visceral and cutaneous afferents

  • few dorsal horn neurons solely devoted to visceral pain processing
  • Cells contacted by dorsal horn neuron won’t be able to distinguish between the 2 possible sites of pain
  • Cutaneous typically dominates since it is most used/recognized
71
Q

major excitatory NT released by primary nociceptive sensory neurons

A

glutamate

72
Q

types of glutamate receptors

A

NMDA, AMPA; ionotropic and activated by glutamate but different time course

  • AMPA = rapid synaptic response
  • NMDA - generate slower excitatory potential and require simultaneous depolarization and glutamate before associated channels open
  • glutamate can evoke both fast and slower excitatory responses from postynaptic dorsal horn neurons depending on whether or not cell is depolarized
73
Q

which part of triple response requires axon vs not

A

Bradykinin actions requires axon, but substance P does not

74
Q

o Stimulation dependent enhancement of post-synaptic response of pain-activated dorsal horn neurons (due to initial activation of AMPA receptors then NMDA)

A

“wind up”

75
Q

Result of activation of NMDA receptors

A
  • triggers series of biochemical cascades leading to long-lasting changes in excitability
  • NMDA phosphorylated by Protein kinase C (PKC) and tyrosine kinases– removes need for depolarization to activate NMDA receptors
76
Q

Intense stimulation of C fibers leads to

A

release of glutamate and substance P

  • Substance P binds to NK1 receptor – closes K channels –> depolarization
  • Sub P lead to enhancement/prolongation of actions of glutamate
77
Q

removal of glutamate and substance P from synapse

A

Glutamate taken up by nerve terminals/glia. Substance P has to diffuse out and interacts with neighboring neurons –>depolarizing and leads to broad central sensitization

78
Q

2 mechanisms for producing analgesia

A

1- gate control mechanism

2- involves descending influences from higher CNS levels

79
Q

Gate control theory

A
  • nociceptive inputs open and
  • balance between nociceptive and non-nociceptive inputs
  • non-nociceptive afferents shut a gate that leads to central transmission of noxious information
  • Essential aspect of gate control theory = anatomical specificity– segments of spinal cord in which nociceptive and non-nociceptive afferent s terminate are inked to same region of body
80
Q

Dorsal Horn Synapse mechanism of analgesia

A

selectively stimulate large diameter Abeta fibers that leads to inhibition of dorsal horn synapse/reduction of pain by exciting inhibitory interneurons that decrease efficacy fof nociceptive dorsal horn synapses
- alternative method for activating Abeta fibers involves stimulation of dorsal columns

81
Q

Descending control mechanism of analgesia

A

stimulation of periaqueductal gray region (PAG) produces powerful analgesia– touch, pressure, and temperature sensations persist and only pain sensation attenuated
- procedure called “stimulation-produced analgesia”

82
Q

where do PAG neurons project

A

nucleus raphe magnus in medulla

83
Q

what NT do PAG neurons release

A

serotonin

84
Q

how to PAG neurons project to spinal cord

A

via dorsal lateral funiculus

85
Q

What does serotonin do in spinal cord

A

serotonin leads to inhibition of second-order neurons of dorsal horn by exciting an inhibitory interneuron

  • Interneuron uses enkephalin as its transmitter (endogenous opiate)
  • Presynaptic inhibition by blockign voltage-gated Ca current
  • postsynaptic inhibition– opens K channels
86
Q

what is located at receptor end of C and Adelta fibers?

A

free nerve endings

87
Q

Substance P release requires what?

A

repetitive stimulation

88
Q

does glutamate release require one stimulus or repetitive

A

one –

89
Q

Activation of NMDA receptors

A

need depolarization and glutamate; once they have been phosphorylated by things in post-syn cell will last a while plus there are more NMDA receptors are put into membrane –> hypersensitivity

90
Q

Dorsal lateral funiculus

A

tract carrying nerve exons from PAG to dorsal horn

91
Q

Opioid receptors

A
  • found throughout CNS/elsewhere
  • G-protein coupled
  • several subtypes– activation leads to inhibition of neuron on which they are found
  • variety of mechanisms involved (inhibit presyn Ca, open K postsynaptically)
  • PAG has a lot of receptors
92
Q

Cannabinoids

A
  • CB1 and CB2 receptors (presynaptic)
  • immune system involved
  • lead to decreased secretion of pro-inflammatory /increased secretion of antiinflamatory agents
  • lead to inhibition of release of neurotransmitters
  • maybe this system also involved in stress-induced analgesia
93
Q

Neuropathic pain

A

persistent pain syndromes– increased responses to noxious stimuli or nonnoxious stimuli

94
Q

Na channels

A

TTX sensitive and TTX resistant

95
Q

Central Mechanisms

A
  • Loss of C fibers or injury in spinal cord –> Abeta fibers grow into area that used to be only C fibers in substantia gelatinosa, so now non-noxious stimuli cause pain
96
Q

Neuropathic pain involvement of immune cells and glia

A

peripheral injury provokes inflammatory reactions at lesions site, DRG, and spinal cord

Neuro Unit 2 (7 decks)

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