lecture 11 part 2 Flashcards
(20 cards)
somatosensory cortex organization
ventral posterior complex –> structures –> secondary somatosensory cortex –> to amygdala and hippocampus
low threshold cutaneous receptors for tactile
OR parietal areas –> to motor and premotor cortical
- size and shape of object
columns
neurons in the primary somatosensory cortex form distinct columns
amputation of digit-
cortex has capacity to rewire - cortical plasticity
in absence of input dendrite needs input so breaks connection and finds a new one
repetitive behavioral task
following repetitive behavioural tasks cortical representation will expand functionally
dynamic range
range of stimulus intensities over which a receptor neutron can encode changes in intensity as changes in neuronal activity
can be reset by adaptation
proprioception receptor type
muscle spindle
afferent axon: large and myelinated b/c require fast feedback loop to let muscles know how hard to contract/relax
touch receptor type
merkel, Meissner, pacinian and Ruffini cells
afferent axon: medium and myelinated (1a/II)
pain/temp receptor type
free nerve endings
afferent axon: AB, C
first and second pain
first pain: sharp, Adelta fiber- myelin
second pain: sustained, dull C fiber - thin and unmyel.
vanillin receptor VR-1
activated by moderate heat >45 degrees
natural ligand: endovanilloids produced in response to injury
also activate in response to capsaicin (child oil)
anterolateral tract
dorsal root ganglion
crosses over contralaterally
- nociceptive pain
antereolateral system
VPN –> somatosensory cortex: where is it, sensory discriminative
amydgala/hypothalamus/PQG: is it unpleasant/ painful?
midline thalamic nuclei- anterior cingulate cortex: affective/motivational (emotion)
visceral pain
relayed by interneurons that are also used to relay surface pain information
can end up with pain coming form surface of body if damage to organs
- midline
summary pain and temp pathways
body:
contralateral cross over immediately
anterolateral system up to VPLateral nucleus
face:
contralateral cross over immediately up to VPMedial nucleus
trigeminal thalamus tract
hyperalgesia
peripheral sensitization - increased sensitivity to pain after injury
allodynia
pain induced by normally innocuous stimulus
pain receptors release peptides to dilute blood vessels and leak serum which increase receptor function and swell
aspirin and ibuprofen reduce PG synthesis
neuropathic pain
spontaneous or damage resulting from afferent fibers
difficult to treat because no initial peripheral point of pain
can arise following amputation
SCN9S- NaV1.7
subtype of sodium channel encoded by SCN9A gene
over responsive: neuropathic pain/ burning
- the hell gene
loss of function: chronic analgesia - insensitive to pain
how do opioids releive pain
by acting in the spinal cord or at PAG
- PAG stimulation is analgesic through actions on brainstem nuclei and other transmitters
central and peripheral
enkephalin containing neuron
increases dorsal horn projection neutron and inhibits nociceptors
gate out C fibres input