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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
Types of acute pain - first vs. second
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
Mechanical nociceptors
Activated by intense pressure: A-beta fibers are blocked first, then A-delta, then C fibers
27
Sensitizers
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
Allodynia
Generation of pain by non-painful stimuli
29
Hyperalgesia
Increased response to painful stimulus
30
Mechanism of the triple response
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
Substance P - Mechanism of release and actions
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
Effects of Bradykinin
Nociceptor activation Vasodilation Increased capillary permeability
33
Mechanism of central sensitization
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
Why does rubbing an injury make it feel better?
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
What is the role of the PAG in pain modulation?
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
Why are SSRIs used to treat pain?
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
What is the sprouting and re-wiring mechainsm of neuropathic pain?
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
How are glial cells involved in neuropathic pain?
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
Which cortical layer receives input from the thalamus in the PCML pathway?
IV
40
Which cortical layer projects to the thalamus?
VI
41
Which cortical layer projects to the basal ganglia, brainstem, and spinal cord?
V
42
Which cortical area receives input from muscle stretch receptors?
3a
43
Which cortical area receives input from cutaneous receptors?
3b
44
Where is myocardium pain referred to?
Upper chest wall, left arm and hand (angina)
45
Where is gallbladder pain referred to?
Scapula
46
Where is uretral pain referred to?
Lower abdominal wall
47
Where is bladder pain referred to?
Perineum
48
Where is appendix pain referred to?
Periumbilical anterior abdominal wall
49
Tabes dorsalis
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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