touch

stimuli: mechanical pressure

receptors: a number of different types of receptors in the skin

  • actually responding on how the world impacts your skin

active vs passive touch: when investigating object w touch we actively move our hands over it, perception is an active process

receptors have different rates of adaptation

  • SA - slowly adapting fibers

  • RA - rapidly adapting fibers

receptors have different sized receptive fields

  • punctate fibers - have small RFs, sharp borders

  • diffuse fibers - large RFs, fuzzy borders

somatosensory and motor cortex:

output: motor cortex (left hemisphere section controls the body’s right side)

input: sensory cortex (left hemisphere section receives input from the body’s right side)

how do we know where our limbs are in space?

  • out flow theory - no

  • joint receptors (tendon organs) - a little

  • cutaneous receptors (responding to the stretching of skin) - a little

  • muscle spindles - yes

pain receptors: nociceptors

  • free nerve endings - 4 types

    • mechanical pain

    • thermal: hot

    • thermal: cold

    • polymodal (any noxious high intensity stim)

    • hot and cold don’t overlap

      • cold also responds to very hot…so an isolated very hot stimulus may seem cold

nociceptors: specialized receptors for pain (noxious stimuli)

  • thermal and mechanical nociceptors

    • separate class for each type of stimulus but only respond to high stimulus

    • thinly myelinated (slower than normal touch, faster than polymodal)

    • associated w sharp/pricking pain

polymodal nociceptors

  • respond to any high intensity noxious stimulus (pressure, temp, chemicals)

  • no myelination (relatively slow; could take 1-3 sec to feel pain from your toe)

  • associated w dull aching/burning pain

transduction? dont know but we think each type of noxious stimulus has a distinct method - can change the threshold to one type of stimuli without effecting threshold of another

hyperalgia: when burn hurts again in warm shower, pain doesn’t adapt

  • when tissue gets damaged blood vessels leak and damaged tissue releases chemicals which produce inflammation

    • histamine directly excited nociceptors

    • prostaglandin lowers threshold of nociceptors

referred pain: pain receptors on organs, share spinal pathway w pain receptors on skin

pain is multimodal: sensation - connection to somatosensory cortex, insula, and anterior cingulate cortex

  • emotional reaction and drive - connections between pain and the hypothalamus and limbic system

watching someone else get hurt and social rejection both activate pain

pain control:

  • NSAIDs (aspirin) - block production of prostaglandin - mostly peripheral effects

  • opioids - bind to opioid receptors in CNS

    • inhibit glutamate and substance P in spinal cord

    • hyperpolize pain cells makes them less likely to find, also impacts throughout the brain

Gate theory of pain: stimulation of touch can block pain signals - inhibition within the spinal cord - top down control

  • analgesia based on gate control theory

    • rubbing painful spot

    • acupressure

    • transcutaneous electrical nerve stimulation

placebo effect has 25-33% reduction in pain

naloxone (no reduction) - blocks endorphins from binding, suggests placebo effect works by producing release of endorphins

mood effects - angry people (opioid issues) have lower thresholds