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Nervous System II > Exteroception & Nocioception > Flashcards

Exteroception & Nocioception Flashcards

1
Q

Short sensory axons

A

Allow receptor potential to spread to synaptic end of the cell by passive electronic transmission

Ex: Rod photoreceptors, auditory hair cells

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2
Q

Long sensory axons

A

Employ regenerative action potentials to carry info from the receptive ending to the synaptic release site in the spinal cord or brainstem

I.e. somatosensory receptors

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3
Q

How do rod photoreceptors detect light?

A

Rod photoreceptors have resting potentials ~-30-40mV due to resting cation conductance via cGMP-gated cation channels

Receptor TM protein rhodopsin binds light-activated 1-trans-retinal, inducing a conformational change in rhodoptsin to metarhodopsin; this stimulates a G-protein which activates cGMP phosphodiesterase; decreased cGMP causes closure of cGMP-gated cation channels, hyperpolarizing the cell; decreased NT release is interpreted by higher order neurons as a response to light

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4
Q

A-alpha afferents

A

Largest diameter
Fastest speed

Muscle spindle and tendon afferents

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5
Q

A-beta afferents

A

Intermediate size
Intermediate speed

Mechanical receptors of skin

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6
Q

A-delta afferents

A

Small size
Slow conducting speed

Sharp pain, cold temperature

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7
Q

C afferent fibers

A 
Smallest diameter (0.2-1.5uM)
Slowest speed (0.4-2m/sec) 
*Unmyelinated

Warm temperature, burning pain, itch, crude touch

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8
Q

Rapidly vs. slowly adapting receptors

A

Rapidly adapting receptors (Meissner, Pacinian) fire only one or a few action potentials when stimulated by steady touch, then stop firing

Slowly adapting receptors (Merckel, Ruffini) fire continuously when stimulated with steady touch

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9
Q

Receptive field

A

The area of the skin in which a mechanical stimulus elicits a response from the individual cell

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10
Q

Merkel’s Disks

A

Slowly adapting afferents with small receptive fields

Present at high density in the finger tips

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11
Q

Pacinian Corpuscle

A

Rapidly adapting afferents with large receptive fields; lie deep in the dermis and subcutaneous tissue

High sensitivity to skin deformation over a wide area, i.e. vibration

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12
Q

Meisner’s corpuscle

A

Rapidly adapting afferents with small receptive fields

Present at high density in the fingertips where they sense fine vibration

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13
Q

Ruffini’s (free nerve) endings

A

Slowly adapting afferents with large receptive fields; lie deep in the dermis and subcutaneous tissue

Evaluate information related to prolonged stretching of skin, i.e. grip

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14
Q

Hair follicles

A

Unmyelinated branches of axons spiral around hair follicles within the dermis; bending of the hair shaft activates the sensory terminals

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15
Q

Ventrobasal complex

A

Ventral posterolateral (VPL) nucleus + Ventral posteromedial (VPM) nucleus in the thalamus

VPL receives input from secondary neurons in the nucleus gracilis and nucleus cuneatus; VPM receives input from secondary neurons in the principal nucleus

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16
Q

Trigeminal mesencephalic nucleus

A

Houses the cell bodies of muscle spindle fibers in the muscles of mastication (proprioceptive afferents) and some mechanoreceptors of the mouth; these cells are the only population of proprioceptive afferents with centrally located cell bodies

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17
Q

Spinoreticular pathway

A

Afferent fibers running within the anterolateral system that convey pain input to the forebrain; elicits emotional/behavioral responses to pain via connections to the limbic system (cingulate gyrus)

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18
Q

Spinomesencephalic tract

A

Afferent fibers running within the anterolateral system that convey pain input to the midbrain periaqueductal gray (PAG)

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19
Q

What is the thermoneutral point?

A

~38 degrees Celcius; neither warmth nor cool sensed because cool and warm receptors have equal firing rates

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20
Q

Cool receptors - firing range & fiber type

A

Firing range: 10-37 degrees C

Cool receptors are mostly A-delta fibers

There are 10x more cool receptors than warm receptors

21
Q

Warm receptors - firing range & fiber type

A

Firing range: 30-48 degrees C

Warm receptors are mostly C fibers

22
Q

Polymodal receptors

A

Located on C fibers; activated by high intensity mechanical, chemical, or thermal stimuli

Includes VR-1 receptor

23
Q

VR-1 receptor

A

Located on polymodal C fiber nerve endings; activated by capsaicin and moderate heat

24
Q

What kinds of molecular receptors detect pain?

A

VR-1: detects capsaicin, H+, and heat

Acid-sensing ion channels (ASICs)

P2X - detect purines (ATP) from dead cells

25
Q

Types of acute pain - first vs. second

A

First pain - immediate “alerting” pain; tolerable and well-localized; carried by lightly myelinated A-delta afferents

Second pain - delayed; throbbing and intolerable, poorly localized; carried by unmyelinated, slowly conducting C afferents

26
Q

Mechanical nociceptors

A

Activated by intense pressure:

A-beta fibers are blocked first, then A-delta, then C fibers

27
Q

Sensitizers

A

Lowers the nociceptor action potential threshold so that weaker stimuli, or even non painful stimuli, evoke pain; cause both allodynia and hyperalgesia

Substance P
Prostaglandins 
ATP
ACh 
5-HT
28
Q

Allodynia

A

Generation of pain by non-painful stimuli

29
Q

Hyperalgesia

A

Increased response to painful stimulus

30
Q

Mechanism of the triple response

A

Tissue damage releases proteases which activate bradykinin; bradykinin vasodilates (causing redness) and increases capillary permeability (causing edema ‘wheel’);

Bradykinin also activates nociceptors, causing pain via C fiber APs which travel centrally toward the cell body and peripherally toward neighboring skin regions; substance P is released from peripheral axon branches in a region surrounding the site of the wound

Substance P causes mild vasodilation (pink ‘flare’) and acts as a sensitizer so that nociceptors within the pink flair are activated more easily (hyperalgesia and allodynia)

31
Q

Substance P - Mechanism of release and actions

A

Released both centrally (near the dorsal horn) and peripherally (in the skin) in response to repetitive stimulation of C fibers by some nociceptive activator (often Bradykinin)

Substance P is both a sensitizer and a vasodilator

32
Q

Effects of Bradykinin

A

Nociceptor activation
Vasodilation
Increased capillary permeability

33
Q

Mechanism of central sensitization

A

Repetitive stimulation of C fibers causes release of Glutamate onto post-synaptic AMPA and NMDA channels as well as release of Substance P onto post-synaptic NK1 channels; Substance P binding causes closure of K+ channels, leading to depolarization; depolarization causes influx of Ca2+ through VSCSs and activates PKC, which phosphorylates NMDA removing the requirement for depolarization

Now, the synapse is potentiated and a single stimulation may be sufficient to evoke a post-synaptic potential even without substance P release; this is hyperalgesia

34
Q

Why does rubbing an injury make it feel better?

A

Rubbing activates non-nociceptive A-beta afferents which synapse on inhibitory interneurons in the dorsal horn; these interneurons synapse on second order neurons in the substantia gelatinosum which receive pain input from afferent C fibers

35
Q

What is the role of the PAG in pain modulation?

A

Periaqueductal gray (PAG) neurons in the midbrain project to the Raphe Magnus in the medulla; Raphe cells project to the spinal cord via the dorsal lateral funiculus, where they release serotonin; serotonin activates inhibitory interneurons which release enkpahalin (an endogenous opiate) onto and inhibit the second-order neurons of the substantia gelatinosum which receive pain input from afferent C Fibers of the ALS pathway

36
Q

Why are SSRIs used to treat pain?

A

SSRIs increase the amount of serotonin available in the spinal cord, where it activates inhibitory interneurons; these interneurons release enkphalin onto the second order neurons of the substantia gelatinosum, which receive pain input from afferent C fibers in the ALS pathway

37
Q

What is the sprouting and re-wiring mechainsm of neuropathic pain?

A

Following nerve injury, A-beta afferents sprout and invade the territory of the substantia gelatinosa where they synapse on second-order neurons of the ALS pain pathway; now, non-noxious stimuli activates pain pathways

38
Q

How are glial cells involved in neuropathic pain?

A

Neuronal damage releases ATP which binds purigenic receptors on microglial cells, stimulating them to secrete BDNF; BDNF down-regulates the potassium/chloride co-transporter (KCC2), which allows accumulation of Cl- within the cell resulting in a more depolarized value for ECl; now, activation of GABA receptors leads to depolarization and excitation, causing hyperalgesia

*Remember: this is a reversion to an embryonic state

39
Q

Which cortical layer receives input from the thalamus in the PCML pathway?

A

IV

40
Q

Which cortical layer projects to the thalamus?

A

VI

41
Q

Which cortical layer projects to the basal ganglia, brainstem, and spinal cord?

A

V

42
Q

Which cortical area receives input from muscle stretch receptors?

A

3a

43
Q

Which cortical area receives input from cutaneous receptors?

A

3b

44
Q

Where is myocardium pain referred to?

A

Upper chest wall, left arm and hand (angina)

45
Q

Where is gallbladder pain referred to?

A

Scapula

46
Q

Where is uretral pain referred to?

A

Lower abdominal wall

47
Q

Where is bladder pain referred to?

A

Perineum

48
Q

Where is appendix pain referred to?

A

Periumbilical anterior abdominal wall

49
Q

Tabes dorsalis

A

Sequelae of neurosyphilia; damage to large diameter myelinated afferent fibers (A-beta) causes hyperalgesia by interfering with the normal ability of these fibers to stimulate inhibitory interneurons in the spinal cord

Nervous System II (12 decks)

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