MT1 Flashcards
somatosensation (4)
- axons?
- touch (mechanical displacement of skin)
- kinesthesis (part of proprioception - position and movement of limbs in space)
- temperature (warm and cold)
- pain (sharp and dull)
- somatosensory receptors are neurons with peripheral (skin) and central axons (spinal cord)
mechanoreceptors
- what kind of skin?
- fast-adapting vs slow-adapting
- small vs large receptive field
4 types
- size, adaptation rate, maximal feature sensitivity, perceptual function
- there are 4 types in glabrous skin (skin with no hair)
fast adapting: stop firing after a bit, may respond again when stimulus gets turned off
slow adapting: firing entire tie stimulus is present
small receptive field: shallow location in skin (epidermis)
large receptive field: deeper location in skin (dermis or subcutis)
- merkel disc: SA 1 - epidermis (shallow)
- slow adaptation rate, small receptive field
- respond best to small slow sustained pressure at very low freq (<5Hz)
- for coarse texture and pattern; fine spatial details - meissner corpuscle: FA 1 - epidermis (shallow)
- fast adaptation rate, small receptive field
- small fast temporal changes (5-50Hz); skin slip
- low freq vibration, grasp stability - Ruffini ending: SA 2 - dermis
- slow adaption rate, large receptive field
- large slow sustained pressure (similar to Merkel but because they’re deeper they need more stimulation to be activated); lateral skin stretch (5-50Hz)
- finger position - pacinian corpuscle: FA 2 - subcutis
- fast adaptation rate, large receptive field
- large fast temporal changes (like meissner but needs larger stimulus) (50-700Hz)
- high freq vibration, fine texture
thermoreceptors
- physiological zero
types of thermoreceptors:
- warmth fibers
- cold fibers
physiological zero: normal skin temperature (30-36 degrees C); no sensations of warmth or cold
thermoreceptors: sense CHANGES in temp
1. warmth fibers increase firing rate when there are increases in skin temperature above 36 deg
2. cold fibers increase firing rate when there are decreases in skin temp below 30 deg
PNS
- what determines conduction speed? (2)
nerve fibers (4)
- diameter
- myelination
- conduction velocity
- receptor type
- inflammatory cells (4 types of chemical receptors)
- double pain
- these 4 different-sized nerve fibers carry somatosensory info to spinal cord (make up PNS) –> speed based on axon diameter and myelination
- A-alpha
- diameter: 13-20um (huge!)
- myelination: LOTS
- conduction velocity: 80-120m/s (very fast!)
- receptor type: proprioceptor - A-Beta
- diameter: 6-12um
- myelination: some
- conduction velocity: 35-75m/s
- receptor type: mechanoreceptor (there are 5 types) - A-Delta
- diameter: 1-5um
- myelination: little bit
- conduction velocity: 5-30m/s
- receptor type: mechanonociceptors (physical stimuli - pain) or thermal nociceptors (temperature - hot/cold)
eg. TRPM8 = thermal nociceptor - C fibers
- diameter: 0.2-1.5 (tiny!)
- myelination: none
- conduction velocity: 0.5-2m/s (very slow)
- receptor type: polymodal nociceptors (pain, temp, itch)
- inflammatory cells release prostaglandin, bradykinin or protons –> activate ion channels)
eg. TRPV1 - capsaicin receptors
note: double pain - A-delta delivers sharp pain, followed by slower throbbing pain from C fibers (lack myelin)
somatosensory receptor transduction
- where does it occur?
- what is channel sensitive to?
- what happens?
- not fully known
- occurs in peripheral axon
- channel sensitive to mechanical force, temperature or chemicals released by injured tissue open; Na+ and Ca+ enter
- neuron depolarizes (receptor potential = slow); action potential travels full length of axon to spinal cord (if threshold level is reached)
dorsal column-medial lemniscal pathway
- cell body location
- axons combine
- layer 2
- DCML path for what?
- 4 synapses (what happens at and after the 2nd one? - 2 nuclei)
- cell bodies of A-beta, C and A-delta fibers are in the dorsal root ganglion (outside of spinal cord)
- many central axons combine into a single nerve trunk and synapse in the dorsal horn of spinal cord (bottom pair comes form feet)
- diff types of somatosensory nerve fibers project to diff layers of the dorsal horn, but layer 2 (substantia gelationosa) gets input from all 3 types of nerve fibers (A-delta, C, and A-beta)
- DCML path = for tactile perception and proprioception (mechanoreceptors) –> for all stimuli below your head (neck to toes)
1. spinal cord (1st synapse for some)
2. medulla (1st synapse for most) - goes up dorsal column from spinal cord and synapses at gracile nucleus (lower body) or cuneate nucleus (upper body))
3. thalamus (lemniscal pathway - info crosses from medulla to contralateral thalamus)
4. parietal cortex (S1 - primary somatosensory cortex)
reflex loop (3 steps)
- noxious stimulus –> info travels to dorsal horn
- interneuron connects sensory and motor neurons
- motor neuron controls movement (withdraw finger)
spinothalamic pathway
- what is it for? (2)
- 3 synapses
S1
- 4 brodmann’s areas
- where do neurons synapse in layer 4?
- which types of mechanoreceptors are in 3b?
- for pain and thermoreception (nociceptors/thermoreceptors)
- for head
- brainstem (1st synapse) - principle sensory nucleus of trigeminal nerve (V)
- thalamus (crossed to contralateral side - 2nd synapse) - ventral posteromedial nucleus
- parietal cortex (3rd synapse) - S1
S1: includes 4 Brodmann’s areas
- 3a (most anterior), 3b, 1 and 2 (most posterior)
- neurons from the thalamus synapse in areas 3a (proprioception) or 3b (touch - mechanoreceptors) in layer 4
- hair follicles, meissner’s corpuscles, and Merkel cells synapse at 3b since they’re mechano (synapses in diff columns according to type)
touch perception
- tactile sensitivity
- discrimination (higher sensitivity? webers fraction? moving stimulus?)
tactile sensitivity: detecting a touch - inverse of absolute threshold (small threshold = high sensitivity)
- highest sensitivity on the face, lowest on the foot
discrimination: JND inc with magnitude of standard stimulus
- JND for touch is smaller for areas of skin with higher sensitivity
- webers fraction = JND/standard (usually 0.02-0.3 for touch)
- moving your finger across = more activation than static touch
homunculus
- what is it?
- example
acuity
- better acuity? (2)
- detection threshold vs 2 point threshold
- example
- each point on skin is represented by a corresponding area in the contralateral cortex but the map is distorted (cortical magnification)
eg. thumb has equal size real estate to forearm even tho thumb is much smaller
acuity: minimum distance at which 2 stimuli are just perceptible as separate (2 point threshold)
- better acuity in skin regions with larger cortical representation, or with smaller receptive fields (they’re more densely packed, and if you want to feel 2 separate points they need to hit 2 separate receptive fields)
- detection threshold can be high when 2 point threshold is low
eg. detection is poor on feet, but if stimulus is strong enough you can have a low 2 point threshold
Aristotle’s illusion
- failure
- success
- result
2 receptive fields close together on cortex may be stimulated at same time, but normal experience has taught us that one object can do this = failure of illusion because we perceive it as one object
2 receptive fields far apart on cortex being stimulated at the same time (normally only happens when 2 objects touch you)
eg. you cross ur fingers and touch with 1 pen = feels like 2 touches
therefore, learning component modifies how we experience touch
somatosensory pathway - temperature and pain
A. skin below head (3)
B. head only (3)
skin below head:
- substantia gelatinosa (1st synapse - in the dorsal horn)
- thalamus (2nd synapse)
- spinal cord neuron that synapses with A-delta and C fibers crosses to other side of spinal cord and travels up to thalamus (goes to ventral posterolateral nucleus)
- same nucleus as DCML touch pathway - parietal cortex (3rd synapse - S1)
head only:
- don’t go to spinal cord, go to medulla (1st synapse) –> go to spinal trigeminal nucleus (same side of body)
- cross over to thalamus (2nd synapse - contralateral ventral posteromedial nucleus - same as spinothalamic touch pathway)
- parietal cortex (3rd synapse - S1)
limbic system
- inputs
- projections
descending pathway
- what is released?
- how? (3)
projections from thalamus to limbic system (anterior cingulate, insula and amygdala) = processing of emotion
- limbic system projects to PFC = role in pain processing - modulate pain experience (eg. emotional experience of chronic pain) –> more than just stimulation of nociceptors/A-delta/C fibers
descending pathway: periaqueductal grey (receives input from PFC) –> sends inputs down –> synapses with C fiber in spinal cord in substantia gelatinosa
- modulates pain sensitivity with enkephalins/endorphins
1. C fiber releases NT substance P
2. substance P membrane receptors (NK-1) on spinal cord neuron - normally signal gets transmitted up to thalamus
3. enkephalins/endorphins block release of substance P
gate control theory
- nociceptive pain
- survival value
- what is gate control theory (how it works)
- example
- descending inputs
nociceptive pain: results from stimulation of free nerve endings in skin, muscles and joints
- survival value: avoid potentially harmful stimuli (reduce injury - learning) and immobilize yourself to promote healing
gate control theory = interaction btwn A-beta touch fibers and slow C and A-delta pain fibers stimulating mechanoreceptor (A-beta) blocks pain gate so that C or A-delta fibers cant synapse with transmission cells (spinal cord neurons) and send signal to brain along spinothalamic path
eg. rubbing sore spot makes it less sore
- descending inputs (central control) also close pain gate (endogenous opiates)
relieving nociceptive pain
- TENS (def + good for?)
- anesthetics (def + local vs general)
- analgesics (def + non-opiate (2) vs opiate)
- acupuncture
- Transcutaneous electrical nerve stimulation (TENS): electric current passed through skin near site of pain = activates A-beta = gate control theory = blocks gate + endogenous opiates released
- good for back pain and childbirth - anesthetics: produce total loss of sensation by interrupting signals travelling to brain
a) local anesthetics: block sodium channels, which neurons need to send APs
b) general anesthetics: act on brain (unconsciousness) - analgesics: painkiller - loss of pain sensations only, not touch; don’t cause unconsciousness
a) non-opiate: mild to moderate pain
i. non-steroidal anti-inflammatory drugs (aspirin/ibuprofen/advil) - block prostaglandin production (binds to C fibers = blocks this level of nociception)
ii. acetaminophen (tylenol) and COX-2 inhibitors (Celebrex) block prostaglandin production without gastrointestinal side effects like i.
b) opiate analgesics: most potent
i. morphine, cocaine, and heroin block nociceptor release of NT substance P and inhibit spinal cord neurons - acupuncture: insertion of long needles into specific places (may release endogenous opiates)