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Somatic sensation includes:
Touch
pain
temperature
proprioception
Skin receptors on glabrous skin include
free nerve endings
meissner corpuscle
merkel’s disk
Ruffini endings
Pacinian
Skin receptors on hairy skin include:
merkel’s disk
ruffini endings
hair follicle receptor
free nerve endings
pacinian
2 layers of skin
epidermis, dermis
Merkel’s disk
light touch
align with top of fingerprint
highest spatial resolution → form and texture
Meissner’s corpuscle
on valleys of fingerprints
fine touch
transducing low frequency vibrations (textured objects moved across skin) 3-40 Hz
grip and sensing slippage
Ruffini endings
sensitive to stretching
determine position of fingers
Pacinian
deep pressure, high frequency vibrations 250-350 Hz (through objects), filter out low frequency stimuli
Receptive field
area of skin innervated by somatosensory nerve ending
small receptive field
merkel’s disk
meissner corpuscles
more sensitive
large receptive field
Ruffini endings
Pacinian corpuscles
less sensitivity
slow adapting
merkel’s disk
ruffini ending
rapidly adapting
meissner corpuscles
Pacinian corpuscles
how are receptors distributed on skin?
The concentration of different receptors differ for each area of the skin depending on the function
ex) high concentration of meissner’s corpuscle on fingertips for fine touch
hair follicle receptor
deflection of hair → EPSP or IPSP
can be fast or slow adapting
guard hairs: more sensitive to deflection
Function of corpuscle
corpuscle: 20-70 concentric layers of connective tissue
continued pressure → layers slip and pressure diffuses → potential dissipate
removing stimulus cause deflexion of axon
→ sensitive to vibrations
Tip of sensory axons
unmyelinated tip with mechanically-gated ion channels
opening of ion channels at tip of sensory axons
stretch axon membrane
force to extracellular protein
force to intracellular protein
two-point discrimination
smallest d between 2 points touching skin at same time where you feel 2 points instead of 1
Primary afferent axons
somatosensory receptors to spine → brain
Pathway
primary afferent axons enter spinal cord through dorsal root ganglia → A beta neurons to:
1) dorsal column → dorsal column nuclei (medulla) - decussation → VP thalamus → S1 (Brodmann’s 3)
2) dorsal horn → second-order sensory neurons (reflexes)
A alpha neurons
proprioceptors of skeletal muscle → reflexive contraction of muscle
muscle spindle
A beta neuron
mechanoreceptors of skin
primary afferent axons
A gamma
pain, temperature
C
temperature, pain, itch
dermatomes
C1 has none because it only as muscle innervation
1:1 correspondence between dermatome and spinal segments
Spinal cord ends at
L3, cauda equina below L3
Cortical areas
Brodmann’s 1, 2, 3
Brodmann’s 3a
recieve projections from VP
proprioception
Brodmann’s 3b
recieve projections from VP
to area 1, 2 (texture and size)
Brodmann’s 1
Texture
Brodmann’s 2
Size, shape
somatotopy of cortex
cortical columns for slow vs rapid adapting neurons
features with higher sensation have more representation on cortex
somatosensory cortex has plasticity depending on
changes in function
Phantom pain
outgoing motor commands but no feedback from muscle spindles → muscle continues to contract at dangerous rates
Pain
nociceptors
Nociceptors are
free nerve endings
K+/Bradykinin/Histamine/Prostaglandins
Temperature
A gamma fiber creates
first pain
sharper, shorter
C fiber creates
second pain
dull, more sustained
temperature
thermoreceptors
thermoreceptor receptor fields
not evenly distributed: cold vs hot spots 1mm wide on skin
each neuron contains one thermoreceptor channel type
what can bind to thermoreceptors
unrelated chemicals
at very high or low temperatures
nociceptors get activated, thermoreceptor activation does not decrease or increase infinitely
Pathway of pain
C fibers → dorsal root ganglion → synapse at zone of lissauer → decussate at spine → (spinothalamic tract) → VP thalamus
Pain afferents contain:
glutamatergic NT (synaptic vesicles)
substance P (storage granules)
only in high frequency stimulation
cause swelling, release of histamines, inflammation, hyperalgesia
Pain sensitization
caused by nociceptors being stimulated by chemicals during inflammation
prostaglandins
bradykinin
histamine (from mast cells)
Hyperalgesia
painful stimuli perceived as more painful
allodynia
pain from normally painless stimulus
pain downregulation pathway
PAG (midbrain) → Raphe nuclei (medulla) → dorsal horn: suppress incoming nociceptive signals
Painkiller placebo
activates the descending control pathway to downregulate pain