sensory physiology Flashcards

1
Q

what are the two schemes peripheral nerves are classified

A
  1. by contribution to a compound action potential (A, B,
    C waves)
  2. based on fiber diameter, myelin thickness,
    conduction velocity (class I, II, III, IV)
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2
Q

what is receptor adaptation

A

when a stimulus persists unchanged for a period of time without a change in position or amplitude, the neural response diminishes or is lost

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3
Q

what kind of stimulation do slow adapting receptors respond to

A

prolonged and constant

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4
Q

what kind of stimulation do fast (rapid) adapting receptors respond to

A

the beginning or end of a stimulus – only active when the stimulus intensity increases or decreases

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5
Q

meissner corpuscle
adaption rate
sensation
receptive field

A

rapid adapting
tap, flutter
small

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6
Q

Pacinian corpuscle
adaptation rate
sensation
receptive field

A

rapid adapting
vibration
large

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7
Q

merkel disk
adaptation rate
sensation
receptive field

A

slow adapting
touch, pressure
small

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8
Q

ruffini corpuscle
adaptation rate
sensation
receptive field

A

slow adapting
skin stretch
large

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9
Q

Pre-synaptic inhibition

A

more powerful form of inhibitory control in all primary afferent fibers
improves brain’s ability to localize signal

actually a diminished excitatory signal:
    Gaba-nergic associated influx of Cl
    hyperpolarization
    decreased Ca influx
    less NT release
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10
Q

what improves the brain’s ability to localize signal

receptive fields

A

pre-synaptic inhibition

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11
Q

steps to cortical processing

A

initial processing of the signal
integration of the initial processing into larger schemes
emotional response to the processing

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12
Q

which cortex layers are enlarged in primary sensory cortex

A

III and IV (main site of termination of axons from the thalamus)

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13
Q

main output neurons

A

pyramidal cells (cortex layer V)

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14
Q

Columns (sensory cortex)
extend
modality
differences with surrounding cells

A

extend through all 6 layers
neurons stacked are fundamentally similar; neurons side
by side are significantly different
columns side by side receive sensory input from same
part of body, but different modalities

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15
Q

S1
location
areas
involved in?

A
post central gyrus
brodman areas 3,1,2
first stop for most cutaneous senses
involved in the integration of information for position 
    sense, size and shape discrimination
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16
Q

S2
location
input
involved in?

A

wall of the sylvian fissure
input from S1
involved in comparison between objects, different
tactile sensatoins, and dtermining whether
something becomes a memory

17
Q

Parieto-temporal-occipital association complex (PTO)

A

High level interpretation of sensory inputs
naming objects
analyzes spacial coordinates of self in environment

doesn’t physically exist, more of a physiological combo

18
Q

what permits focusing activities

A

S1 sending projections back down to subcortical structures (most often thalamus)
descending corticothalamic axons > ascending
thalamocortical axons

19
Q

what links the primary and association areas of the sensory cortex and allows for simultaneous processing of multiple sensations

A

cortico-cortical projections (parallel paths of sensation)

can be ipsi or contra

20
Q

what are corticofugal signals and what do they do

A

transmitted back from cortex to lower relay stations (thalamus, medulla, SC)
controls intensity of sensory sensitivity
typically inhibitory and suppresses sensory input

21
Q

doctrine of specific nerve energies

A

no matter where along the afferent pathway is stimulated, sensation felt is determined by receptor the pathway is for

22
Q

law of projections

A

no matter where along the afferent pathway is stimulated, perceived sensation is from origin of sensation

23
Q

silent nociceptors

A

related to phenotype switching – rarely stimulated sensory receptors can undergo phenotype switching to become another modality receptor?)

24
Q

nociceptor axons

A

slowly conducting unmyelinated (C fibers)
thinly myelinated (Abeta fibers)
w/ free endings

25
Q

peptidergic free nerve endings
express
responsive to

A
substance P (SP) and calcitonin gene-related peptide (CGRP)
responds to nerve growth factor (NGF)

most visceral afferents
half of cutaneous afferents
chronic inflammation
visceral pain

26
Q

non-peptidergic free nerve endings
express
responsive to

A

not any of the neuropeptides
responds to glial-derived neurotrophic factor (GDNF)

few visceral afferents
half of cutaneous afferents
diabetic neuropathy

27
Q

receptors that sense noxious stimuli

A

TRP receptors

ligand-gated permeable to Ca, Na, and/or K (mostly Ca)

28
Q

TRP receptors and what they sense

A

TRPV1 – capsaicin (extreme hot)
TRPA1 – spices (extreme cold)
TRPM8 – menthol

29
Q

what modulates nociceptors

A

descending systems and interneurons in the dorsal horn

30
Q

local system of modulating nociceptors

A

gate control theory of pain (rubbing spot that hurts to ease pain)

absence of input from slow pain C fibers, active interneurons (activated by Adelta fiber) inhibit/suppress pain pathway (uses gly)

31
Q

descending inhibition of modulating nociceptors

A

dampens input on its way to the cortex

32
Q

pathway of descending inhibition

A

PAG activated by opiates, EAA, and cannabinoids
descending projections –> Locus coeruleus [pons] (NE)
and Raphe nucleas [medulla] (5-HT)
5-HT and NE released into dorsal horn activates
inhibitory interneurons and supress spinothalamic
projection neurons
local inhibitory interneurons release opiods
(Enkephalin)
opiates activate mu-receptors on pre and post-synaptic
terminals of C fibers
=reduction of release of SP from C fiber and reduces
nociception

33
Q

Bradykinin effects on nociception

A

in chronic inflammation, bradykinin increases expression of NGF which –> increase in peptidergic free nerve endings –> increase nociception

34
Q

which cortex is important in interpretation of nociception

A

insular cortex
integrates all signals related to pain
process info about internal state of body

35
Q

what brain structure is important in the emotional component to pain

A

amygdala

36
Q

where does visceral input go to

A

hypothalamus and medulla

37
Q
stimuli adequate to induce nociception 
(mechanical, chemical, thermal)
skin 
joints 
muscle 
viscera
A

skin: all 3

joints muscle viscera: mechanical and chemical

38
Q

why is referred pain a thing?

what is antidromic signaling

A

brain requires experience to localize pain
visceral pain is not experienced enough to have trained the brain

antidromic signaling further diffuses pain across multiple organs