Phys - Sensory Phys Flashcards
what is the largest and fastest sensory (affarent) fiber type of the peripheral nerve fibers and where is its receptor
- what classification of fiber is it
A-alpha
primary muscle spindles and golgi tendon organ
- class Ia and Ib
what is the smallest and slowest sensory (affarent) fiber type of the peripheral nerves and where is its receptor
- what classification of fiber is it
C fibers
skin mechanoreceptors, thermal receptors, nociceptors
- class IV
what type of fiber is A-beta fibers, what class, and where are its receptors
sensory
class II
secondary muscle spindles, skin mechanoreceptors
what type of fiber is A-delta fibers, what class, and where are its receptors
sensory
class III
skin mechanoreceptors, thermal receptors, nociceptors (same as C fibers)
where are the receptors for A-alpha motor fibers
extrafusal skeletal muscle fibers
where are the receptors for A-gamma motor fibers
intrafusal muscle fibers
what type of fiber are B fibers
- where are their receptors
motor (efferent) fibers
preganglionic autonomic fibers
where are the receptors for C motor fibers
postganglionic autonomic fibers
what sensory system does not relay information through the thalamus on its way to the cerebral cortex?
olfactory
in somatosensory systems, what nuclei corresponds to the body and what corresponds to the face
body: VPL
face: VPM
describe receptor adaptation
when a stimulus persists unchanged for several minutes without a change in position or amplitude, causing the neural response to diminish and sensation to be lost
compare slowly and rapidly adapting receptors
slowly: respond to prolonged and constant stimulation
rapidly: respond only at the beginning or end of stimulus (when stimulus intensity increases or decreases)
what cells of the skin are responsive to taps or flutters
- what is the receptive field size?
meissner’s corpuscles
- small receptive field size
what cells of the skin are responsive to motion and direction
hair follicle receptors
what cells in the skin are responsive to vibration?
- what is their receptive field size?
pacinian corpuscles
- large receptive field size
what cells of the skin are receptive to touch and pressure?
- what is their receptive field size?
merkel discs
- small receptive field size
what cells of the skin are responsive to skin stretching?
- what is their receptive field size?
ruffini corpuscles
- large receptive field size
what kind of response (slowly or rapidly) do meissner’s corpuscles have to stimulation?
rapidly adapting
what kind of response (slowly or rapidly) do pacinian corpuscles have to stimulation?
rapidly adapting
what kind of response (slowly or rapidly) do merkel cells have to stimulation?
slowly adapting
what kind of response (slowly or rapidly) do ruffini corpuscles have to stimulation?
slowly adapting
what kind of response (slowly or rapidly) do hair follicle receptors have to stimulation?
rapidly or slowly adapting
where is tactile acuity for 2 point discimination the highest and lowest
highest: fingertips and lips (smallest receptive fields)
lowest: calf, back, and thigh (largest receptive fields)
how does pre-synaptic inhibition occur
GABA causes influx of Cl- into axon –> hyperpolarization occurs –> less Ca2+ enters cytosol –> less NT release
what is the purpose of pre-synaptic inhibition
improves brain’s ability to localize the signal
what layers of the cortex are enlarged because they are the primary sensory cortex and are the main site of termination of axons from the thalamus
III and IV
in the cortex, compare neurons stacked above and below each other
- compare neurons stacked side by side
above and below: fundamentally similar
side by side: significantly different
what layer of the cortex do input signals first enter
layer IV
function of primary somatosensory cortex (S1) and where is it located
integration of information for positional sense and size and shape discimination
- located in the post-central gyrus
function of secondary somatosensory cortex (S2) and where is it located
comparisons between objects, different tactile sensations and detmeining whether something becomes a memory
- wall of sylvian (lateral) fissure
function of PTO (parieto-temporal-occipital association complex)
- analyzes spatial coordinates of self in environment
- names objects
- high level interpretation of sensory inputs
what is the significance of the primary sensory cortex sending projections (axons) back down to subcortical structures like the thalamus
permits increased focusing activities
function of cortico-cortical projections
they establish parallel paths of sensation
- allows for simultaneous processing of multiple sensations
function of corticofugal signals
inhibit and suppress sensory input in order to prevent getting overwhelmed with senses
- controls intensity of sensory sensitivity
what is the doctrine of specific nerve energies
if an afferent pathway is stimulated at any point, the sensation that occurs is determined by the sensory receptor in the periphery that is connected to that afferent pathway
- ex: light touch is perceived no matter where along the afferent pathway is stimulated
what is the law of projections
if anywhere along an afferent pathway is stimulated, you will get sensation in the origin of sensation
- you can stimulate anywhere along an afferent pathway, but you will still get sensation in the right thumb (if that’s where the origin of sensation is)
compare pain and nociception
pain: feeling unpleasant sensory info
nociception: neural process of encoding the painful stimuli
what are the autonomic and behavioral consequences of nociception
autonomic: increased BP
behavioral: motor withdrawal reflex
describe how sharp, acute pain occurs and then dull, throbbing pain after time has passed
combination of A-alpha fibers and C fibers
- A-alpha fibers respond and transmit the sharp, acute pain, and after time C fibers transmit the dull, throbbing pain
describe the two types of phenotype switching for nociceptors
1) silent nociceptors get stimulated during a chronic inflammatory condition and genetically switch to a new type of nociceptor
2) non-nociceptors become nociceptors
decribe free nerve endings
axons with peripheral terminals that are not associated with specific structures or cell types
- lack specialized receptor cells or encapsulations
describe peptidergic free nerve endings
- what growth factor are they responsive to
free nerve endings that express neuropeptides (substance P and CGRP)
- responsive to nerve growth factor (NGF)
most visceral affarent fibers have what type of free nerve ending
peptidergic
(responsive to NGF)
describe non-peptidergic free nerve endings
- what factor are they responsive to?
free nerve endings that do not express neuropeptides
- responsive to glial-derived neurotrophic factor (GDNF)
what type of free nerve endings are associated with chronic inflammation
peptidergic
(chronic inflammation causes up-regulation of NGF, which peptidergic nerve endings are responsive to)
what type of free nerve endings are associated with diabetic neuropathy
non-peptidergic
(diabetic neuropathy causes changes in non-peptidergic nerve endings)
what type of channels are activated by TRP receptors
ligand-gated non-selection cation channels permeable to Ca2+, Na+, and K+
what TRP receptor responds to capsaicin (hot peppers) and hot temperatures
TRPV1
what TRP receptor responds to menthol and cold temperatures
TPRM8
what TRP receptor responds to allyl isothiocyanate (mustard and radishes) and cold temperatures
TYPA1
how does ATP activate nociceptors
via P2X channels
how does H+ activate nociceptors
via ASIC (acid sensitive channels)
how do substance P (SP) and calcitonin gene-related peptide (CGRP) activate nociceptors
they are released by nociceptors and then come back to activate the nociceptors even further
what inflammatory mediators can activate nociceptors
histamine and bradykinin
what neurotransmitters do C fibers release in the synapse with second order neurons in the spinal cord
EAA (which binds to non-NMDA receptors) and SP/CGRP (peptidergics)
what neurotransmitters do A-delta fibers release in the synapse with second order neurons in the spinal cord
EAA (binds to non-NMDA receptors)
how is the pain pathway suppressed when there is no pain sensed
in absence of input of C fibers, a tonically activa inhibitory interneuron suppresses the pain pathway (blocks nocicpetive signal from continuing to move foward)
describe the gate control theory of how strong pain causes strong painful stimulus to the brain
painful stimulus travels through a C fiber –> the C fiber inhibits the inhibitory interneuron –> a strong signal is sent to the brain
using the gate control theory, explain how rubbing one’s elbow can reduce the sensation of pain felt after hitting the elbow
the hitting of the elbow causes inhibition of the inhibitory interneuron, but the rubbing action is a non-painful stimulus which travels through A-beta fibers to stimulate the inhibitory interneuron by releasing EAA
–> the inhibitory interneuron releases glycine and inhibits the secondary sensory neuron of the nociceptive pathway, decreasing the pain felt after bumping your elbow
how does descending inhibition decrease nociception
opiates, EAA, and cannabinoids activate PAG –> PAG activates locus ceruleus and raphe nucleus –> NE and serotonin are released into dorsal horn and activate inhibitory interneurons –> interneurons release opiates and activate mu receptors on pre-synaptic terminals of C fibers –> reduction of SP from C fibers and less nociception
what are the two options for serotonin and NE to inhibit inhibitory neurons in descending inhibition of nociception
1) direct inhibition
2) activation of intermediate neuron that releases opiates that will inhibit nociception
function of bradykinin in inflammatory states
bradykinin directly activates nociceptors and also upregulates NGF, which will then activate even more nociceptors and cause more pain
where is most nociception processed
insular cortex
what functions does the insular cortex provide to process nociception
- processes info about the body viscera
- autonomic responses to pain
- integrates all signals related to pain
damage to the insular cortex causes what
asymbolia
- sensation of pain but without emotional unpleasantness
function of amygdala
fear, emotional component of pain
what stimuli are adequate to activate nociceptors in the skin
thermal
mechanical
chemical (formalin, carrageenan, bee venom, capsaicin)
what stimuli are adequate to activate nociceptors in the joints
mechanical
chemical (inflammatory, other mediators)
what stimuli are adequate to activate nociceptors in the muscles
mechanical
chemical: inflammatory)
what stimuli are adequate to activate nociceptors in the viscera
mechanical (distension, traction on mesentery)
chemical (inflammation, mediators)
describe the pain associated with cutaneous damage like cuts and burns
fast, sharp pain followed by slow, dull pain
describe the pain associated with ligamentous and bone pain
dull and achy
- associated with muscle spasm
describe the pain associated with injury or ischemia to muscle
both fast and slow pain
describe the pain associated with the internal visceral organs
poorly localized, very sensitive to stretch
why does referred pain occur
the brain requires experience to localize pain, and visceral pain is not experienced enough in early development to train the brain to localize its pain
