Exam 2: Pain, Temp, & Itch

Question 1

First pain nociceptors

Answer 1

Aẟ fibers

Question 2

Second pain nociceptors

Answer 2

C fibers

Question 3

TRP Channels

Answer 3

Family of receptors sensitive to heat and cold, Selective cation channels

Question 4

TRPM8

Answer 4

responds to decreases in temperature < 28 deg. C Also activated by menthol, eucalyptol, icilin

Question 5

TRPV1

Answer 5

responds to heat and capsaicin, but not cold or menthol

Question 6

Nav 1.7 and mutations

Answer 6

Nav1.7 (subtype of sodium channel) important for the transmission of nociceptive information: Mutations of NAV1.7 can lead to the inability to detect noxious stimuli, Hyperexcitability of channel

Question 7

Nav 1.8

Answer 7

NAV1.8 gene expressed in most C fiber nociceptors, Transmits noxious mechanical and thermal information

Question 8

Why can grasshopper mice eat scorpions

Answer 8

Grasshopper mice have evolved a mutation in their Nav1.8 channels that leads to analgesia

Question 9

Central pain pathway

Answer 9

anterolateral column/spinothalamic tract

Question 10

anterolateral column

Answer 10

Cell bodies in DRG, axons enter the dorsal horn. 2nd order neurons in Rexed’s laminae: C fibers terminate in I & II, Aẟ fibers terminate in I and V. Axons decussate in the spinal cord and form the anterolateral pathway

Question 11

Spinothalamic tract

Answer 11

Nociceptive info remains segregated from other somatosensory input in the thalamus and SI.

Question 12

Pathway for pain and temperature from the face

Answer 12

First-order neurons: Located in the trigeminal ganglion, Enter pons and descend to medulla / spinal trigeminal tract, Terminate in the spinal trigeminal nucleus
Second-order neurons: Decussate in medulla, Trigeminothalamic tract, Terminate in the VPM of the thalamus
Third-order neurons: Travel from VPM of the thalamus to S1

Question 13

Pathway for visceral pain

Answer 13

Info travels through the dorsal column, Synapse on dorsal column nuclei of the medulla, Form contralateral medial lemniscus

Question 14

What is referred pain and what is the likely underlying cause?

Answer 14

Some neurons in Rexed’s lamina V receive converging inputs: Nociception, Non-nociceptive somatosensory, Visceral sensory
Likely underlying cause: pain that arises from damage to visceral organs but is perceived as coming from a somatic location

Question 15

Peripheral mechanisms of sensitization

Answer 15

Tissue injury cause release of inflammatory mediators (“inflammatory soup”) Inflammatory mediators depolarize nociceptor nerve endings

Question 16

Central mechanisms of sensitization

Answer 16

Increase in the excitability of neurons in the dorsal horn (second-order neurons) following high levels of activity in the nociceptive afferents, Triggered by activity in nociceptors and/or mechanoreceptors

Question 17

Hyperalgesia

Answer 17

nociceptors give a larger response to noxious stimuli

Question 18

Allodynia

Answer 18

induction of pain by a normally innocuous stimulus

Question 19

Phantom limb pain—cause, treatment:

Answer 19

Reorganization of S1 and subcortical somatosensory centers so that neurons representing the missing body part respond to mechanical stimulation of other body parts

Question 20

Placebo affect and endorphin activation:

Answer 20

Physiological response following an inert remedy

There is a physiological basis for pain relief

Question 21

Gate theory of pain

Answer 21

Perception of pain is the subject of central modulation
Henry Beecher—Military doctor during WWII, observed and reported on 225 soldiers with severe wounds. 75% of these soldiers had so little pain that they did not ask for pain relief. Perception of pain depends on context

Question 22

Endogenous opioids and modulation of pain in the dorsal horn:

Answer 22

Exogenous opioids are powerful analgesics (e.g., morphine)
Opioid receptors located in most (if not all) brain areas involved in modulating pain
Endogenous opioids modulate nociceptive info at the first synapse in the dorsal horn

Question 23

Endocannabinoids and modulation of pain

Answer 23

Retrograde signaling, Decrease release of NTs (e.g., GABA, glutamate), Modulate neuronal excitability
Analgesic effects of PAG stimulation blocked by CB1 antagonists, Exposure to noxious stimuli increases the level of endocannabinoids in PAG

Question 24

3 main types of pruriceptors:

Answer 24

Histaminergic, Non-Histaminergic, and Mechanoreceptors
Itch and pain can be produced by stimuli of the same modality (e.g., mechanical, thermal, chemical, and electrical)
Low intensity stimuli: itch Higher intensities: pain
loss of itch sensation is paralleled by the loss of pain sensitivity

Question 25

Are pain and itch mediated through the same pathway?

Answer 25

Some evidence suggests that pain and itch are mediated through the same pathway, some suggests that they are mediated through distinct pathways