sensory processing touch & pain

labeled lines

separate nerve tracts
various receptor cells send information to the somatosensory cortex through labeled lines

free nerve endings

pain and temperature

TRP receptor family

pain

thermoreceptors

temperaturemes

meissner corpuscles & merkel’s disc

light and fine touch

meissner corpuscles are

dynamic and rapidly changing

merkel discs are

slow adapting

pacinian corpuscle

vibration and pressure

ruffini endings

stretch

touch and pain fibers are

smaller

proprioception fibers are

larger

A alpha fibers

proprioception
receptor type: muscle spindleA

A beta fibers

touch

receptors: pacinian corpuscles, Ruffini’s endings, merkel’s discs, messiner corpuscles

A delta fibers

pain; temperature

receptor: free nerve endings

C fibers

temperature, pain, itch

receptor: free nerve endings

range fractionation

mechanoreceptors with different activation thresholds and sensitivities, so each one is tune to a specific portion of the stimulis range

low threshold receptors

meissner, merkel

high threshold receptors

pacinian, ruffini

coding

patterns (number, frequency/ rhythm) of action potentials that represent a stimulus

levels of sensory processing

spinal cord → brainstem → thalamus → primary sensory cortcial areas/ seconday sensory cortex

second order

spinal cord → brainstem

brainstem → thalamus

somatosensory pathway

dorsal column system delivers touch information to the brain

somatosensory at level of medulla

synapse on dorsal column nuclei in the medulla

axons from neurons in the medulla cross the midline and go to the thalamus

somatosensory from thalamus

directed to primary somatosensory cortex (S1)

primary somatosensory cortex

receives information from the opposite side of the body

homunculus

large hands, mouth, tongue, ears, and face

secondary somatosensory cortex

receives it main input from the primary cortical area for that sense

multimodal neurons integrate touch information as a unfirom sense

nociceptors

peripheral receptors on free nerve endings that respond to painful stimuli

when tissue is injured,

affected cells release chemicals that can activate nociceptors

eg serotonin, histamine, various enzymes and peptides

capasicin

compound responsible for the "hot” in chili peppers

binds to TRPV1 channel

TRPV1 channel

detect painful heat; chili peppers evolved capasicin to ward off mammalian peppers

TRPV1 receptors are on

thin, unmyelinated C fibers

conduct more slowly, producing lasting pain

dull ache

TRP2 receptor

detects even higher temperatures

does not respond to capsaicin

TRP2 receptors on

large myelinated A delta fibers

conduct very rapidly (<0.1s)

sharp pain

injured cells release

substances that cause local inflammation and stimulate nerve endings

histamine

activates pain transmitting nerve fibers and induces release of neuropeptides that cause pain

excess histamine

joint pain (arthritis)/ MSK/ connective tissue pain (fibromyalgia)

substance P

neuropeptide produced in the soma peripheral neuron cell bodies → contributes to pain

substance P is produced by

DRG neurons and package into dense core vesicles which undergo fast axonal transport and its release requires strong repetitive stimulation → persistent/ intense pain

anterolateral (sphinthalamic system)

transmits sensations of pain and temperature to the brain

substance P tells us

how much pain is present

pain pathway
from the DRG →

synapse on second order neurons that project across midline, before ascending to the thalamus

pain information is integrated in the

cingulate cortex

extent of activation in cingulate correlates with

how much discomfort different people report in response to same mildly painful stimulus

itch and pain are encoded by

distinct but interacting circuits → labeled lines

nociceptors transmit

pain information
substance P and glutamate stimulate pain neurons which project to the pain

pruriceptors

express TRP channels responsive to irritants/ allergens and transmit itch information via stimulation of gastric-releasing peptide (GRP) neurons

pruriceptors are linked to

nociceptors via bHLHb5+ inhibitor interneurons

pain can inhibit

itch
bhihbt+ inhibits GRP/ GRPR

pain information crosses

midline in the spinal cord, before ascending to the thalamus
A delta and C fibers

anterolateral system transmits

sensation of pain and temperature

pons

relay of sensory and motor info; breathing and sleep

reticular formation

network of brainstem nuclei; arousal, consciousness, circadian rhythm, sleep-wake cycles, coordination of somatic motor movements, cardiovascular and respiratory control, pain modulation and habituation

periaqueductal gray

modulation and perception of pain

periaqueductal gray receives information from

A delta fibers but not C fibers

pain information integrated in

cingulate cortex

extent of activation in cingulate correlates

how much discomfort different people report in response to same mildly painful stimulus

subregions of cingulate for

emotional vs sensory aspects of pain

periaqueductal gray

area in the midbrain involved in pain perception

electrical stimulation of the PAD produces

potent analgesia

PAG neurons send

endorphin-containing axons to medulla

medullary neurons send axons to spinal cord, stimulating neurons to release endogenous opioids

TRP are

non-selective cation channels

nociception

processing of afferent information related to tissue damage p

pain

unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

fibers in pain transmission

a delta

c fibers

serotonin plays a role in

modulation of pain

sensitize or relieve pain

at site of injury, mast cells

secrete 5-HT which then promotes hyperalgesia

serotonin in pain pathway orginates from

periaqueductal gray

raphe nuclei (rostral ventromedial medulla)

5-HT 1 receptors are

inhibitor (Gi)

5HT 2 receptors are

excitatory (G alpha S)

5 HT 3

excitatory

CNS/ PNS

itch response

5HT7

inhibitor

analgesia

brain lacks

nociceptors

trigeminal system

can secrete CGRP → increase activity of receiving cell

CGRP

neuropeptide, released from trigeminal nerves → migraine pain

some migraines are associated with a wave of

hyper excitation followed by cortical spreading depression

stress can

activate anagesia systems as well as heighten pain

brain systems produce analgesia

pain threatens to overwhelm effective coping strategies

increased activity of amygdala

increased 5HT release

complex regional pain syndrome

idiopathic condition that causes high levels of pain

type 1 CRPS

without nerve damage

type II CRPS

after known nerve damage

epidermis

free nerve endings

merkel’s disc

meissner corpuscle

hypothermis

ruffini ending

pacinian corpuscle

as a stimulus intensity increases

the firing rate of mechanoreceptor afferent nerve increases

light touch has _ firing frequency

low

strong pressure has _ firing frequency

high

nociceptors

peripheral sensory receptors that respond to tissue damage and relay information to the CNS

first level of sensory processing

receptors (sensory cranial/ peripheral nerves) → spinal cord

3rd level of sensory processing

thalamus → sensory cortex