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Neuro test 2 > 11. Sensory Physiology > Flashcards

11. Sensory Physiology Flashcards

1
Q

LO1: What are the classification systems for peripheral axons?

A
  1. Their contribution to a compound AP (a, b, and c WAVES) recorded from an entire mixed peripheral nerve
  2. Based on FIBER diameter, myelin thickness, and conduction velocity of an AP (classes 1,2,3, and 4)

~compound AP and conduction velocity of nerve fibers= often used as diagnostic tests in evaluation of peripheral nerve disease~

~conduction velocity determines fibers contribution to compound AP~

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2
Q

LO2: What electrophysiologic classifications are there of sensory afferent vs. motor efferent fiber types:

A

Sensory: A and C
(Aa, Ab, Ad, C)

Motor: A, B, and C
(Aa,Ay, B, C)

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3
Q

LO2: Aa- What subtype does Aa sensory afferent have? What is the fiber diameter? what is the conduction velocity?

A

1a and 1b

BIGGEST AND FASTEST

(monitor body in space, primary muscle spindles, golgi)

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4
Q

LO2: C- What subtype does C sensory afferent have? What is the fiber diameter? what is the conduction velocity?

A

4

smallest and slowest

(skin mechanoreceptors, thermal receptors, nociceptors)

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5
Q

LO 3: What is generator potential?

A

an appropriate stimulus applied to a somatosensory receptor produces this, which when large enough, leads to APs that can be carried over a considerable distance into the CNS

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6
Q

What do all (but one) sensory systems go through? which doesnt?

A

all sensory systems are going to route through thalamus EXCEPT olfactory

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7
Q

LO3: what is convergence?

A

if have second order neuron gets input from two separate first order neurons= convergence

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8
Q

LO3: what is divergence?

A

if you have a given peripheral afferent, the central processes might synapse on second order neuron; but if has branches of primary afferent, then branches might synapse on different second-order sensory neurons

One first order neuron –> two 2nd order neurons

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9
Q

What is the relationship between sensory receptors and intensity of stimulus?

A

number of active receptors INCREASES with increased intensity of the stimulus (amplitude of receptor potential)

makes digital pulse code (freq of APs is proportional to intensity of stimulus)

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10
Q

What is receptor adaptation?

A

when stimulus persists unchanged for several minutes, without change in position or amplitude, neural response diminishes and sensation is lost

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11
Q

LO4: What is a rapidly-adapting (RA) receptor?

A

receptors that respond only at the beginning or end of a stimulus; basically active when stimulus intensity increases or decreases; rapidly adapts then stops; stimulus withdraws, get activity

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12
Q

LO4: What is a slowly-adapting (SA) receptor?

A

receptors that respond to prolonged and constant stimulation

persists entire duration of stimulus

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13
Q

LO4: Which mechanoreceptors are RA receptors?

A

Meissners corpuscles, Pacinian corpuscles, and hair follicle receptors

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14
Q

LO4: Which mechanoreceptors are SA receptors?

A

Ruffini ending, Merkel cell-neurite complexes, tactile free nerve endings, hair follicle receptor

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15
Q

LO4: Which mechanoreceptors are SA+ RA receptors?

A

hair follicle receptors

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16
Q

LO4: What kind of sensation is produced by microstimulation of Meissners corpuscles (RA)? What is their receptor field size?

A

tap, flutter

small receptive field

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17
Q

LO4: What kind of sensation is produced by microstimulation of Hair follicle receptors (RA/SA)?

A

motion, direction

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18
Q

LO4: What kind of sensation is produced by microstimulation of Pacinian corpuscles (RA)? What is their receptor field size?

A

vibration

large receptive field

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19
Q

LO4: What kind of sensation is produced by microstimulation of Merkel disks (SA)? What is their receptor field size?

A

touch, pressure

small receptive field

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20
Q

LO4: What kind of sensation is produced by microstimulation of Ruffini corpuscles (SA)?

A

skin stretch

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21
Q

LO5: What is the significance of receptive fields?

A

individual mechanoreceptor fibers conveying information from a limited area of skin (receptive field)

physical innervation in given quadrant of skin

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22
Q

LO5: Does receptor adaptation determine receptive field size?

A

NO

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23
Q

LO5: what is 2-point discrimination?

A

allows for spatial resolution of detailed textures in areas of body that need high tactile acuity

highest on fingertips and lips (bc afferents have smallest receptive fields)

lowest on calf, back, and thigh (largest receptive fields)

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24
Q

LO5: What are the two paths of receptive field perception?

A

2 receptive fields with convergence–> one signal goes to brain

OR

same distance and stimulate 2 different receptive fields but could go and split into two different signals to be perceived separately (more processing that can occur)

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25
LO6: What is pre-synaptic inhibition? What does it improve
primary afferent Neurotransmission is controlled by pre-and post-synaptic inhibitory mechanisms probably more powerful form of inhibitory control diminished excitatory signal Improves brains ability to localize the signal!!
26
LO6: How does pre-synaptic inhibition occur?
1. GABAergic associated influx of Cl- into axon 2. Hyperpolarization 3. Less Ca2+ enters cytosol 4. Leads to less NT release from presynaptic terminal
27
LO6: Where can presynaptic inhibition occur?
can repeat all the way to the cortex, further narrowing down the signal
28
What are the steps of cortical processing?
1. Initial processing of signal 2. Integration of initial processing into larger schemes 3. Emotional response to processing
29
What is the arrangement of the cortex?
has 6 layers 3 and 4 are enlarged in primary sensory cortex (main site of termination of axons from thalamus) main output neurons = pyramidal cells
30
LO8: What is the significance of columnar organization to the cortex?
third spatial dimension of cortex (z)= depth neurons stacked above and below eachother are fundamentally similar (by functionality), but neuronal columns side by side are significantly DIFFERENT columns extend through all 6 layers each column deals with one sensory modality in one part of the body neighboring columns receive sensory info from same part of body but different sensory modality
31
LO8: What is the primary input layer into the sensory cortex?
into layer 4 via thalamus
32
LO7: What is the normal function of Primary somatosensory cortex (S1) in sensory perception?
located in post-central gyrus; Brodmann area 3, 1, 2 ; first stop for most cutaneous senses; somatotopic representation ANSWER: involved with integration of the info for position sense as well as size, shape discrimination
33
LO7: What is the normal function of secondary somatosensory cortex (S2) in sensory perception?
located in wall of sylvian fissure; input from S1; somatotopic representation (less detailed); cognitive touch ANSWER: comparisons bw objects, different tactile sensations, and determining whether something becomes a memory
34
LO7: What is the normal function of parieto-temporal-occipital association area (PTO) in sensory perception?
high level interpretation of sensory inputs, receives input from multiple sensory areas, analyzes spatial coordinates of self in environment, names objects, and more
35
What can the primary sensory cortex do with its projections?
can send projections back down to subcortical structures, most often to thalamus descending corticothalamic axons > ascending thalamocortical axons (suprising) permits focusing activities; oscillating
36
What are cortico-cortical projections (not as impt)?
production that is of one cortex, hops to other establishes parallel paths of sensation links primary and association areas of sensory cortex vision, audition, and somatic senses establish hierarchy within the system allow for simultaneous processing of multiple sensations can be ipsilateral or contralateral hemispheric connections (via corpus callosum)
37
What are corticofugal signals?
transmitted back from cortex to lower relay stateions in thalamus, medulla, or spinal cord running away from cortex!! controls intensity of sensory sensitivity typically inhibitory and SUPPRESSES sensory input (suppress other senses so don't get overwhelmed with sensory overload); keep tone down
38
LO9: How does the law of specific nerve energies impact how/what a person perceives?
no matter where along afferent pathway is stimulated, sensation that will occur is determined by the nature of the sensory receptor in the periphery connected to that pathway
39
LO9: How does the law of projection impact how/what a person perceives?
L.O.P- transmits information of where pathway is stimulated no matter where along afferent pathway is stimulated, the perceived sensation arises from the origin of the sensation
40
LO10: What is the difference bw pain and nociception?
Pain- unpleasant sensory or emotional experience associated with actual or potential tissue damage ; also an emotional reaction/experience!! Nociception- neural process of encoding noxious stimuli (damaging or threatening stimuli); consequence can be autonomic or behavioral; pain sensation not necessarily implied.
41
LO11: What is fast vs. slow pain, what fibers involved that cause it??
two nociceptor fibers that transmit pain A-delta: have more myelin--> faster signal transmission C-fibers: less myelin--> slower transmission together : sharp, acute pain--> dull, throbby pain
42
LO12: Under what conditions are nociceptors activated?
Nociceptors: high threshold sensory receptor of peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli
43
What are the 4 different types of pain?
somatic or cutaneous pain muscle pain deep/bone pain visceral pain
44
What can pain be characterized as?
thermal, mechanical, chemical many subtypes of each many polymodal (respond to more than one pain characteristic)
45
LO12: What are silent nociceptors and phenotype switching?
silent nociceptors are related to phenomenon of phenotype switching (so rarely stimulated that eventually if something happens, then that can change genetic expression of recepters on what normally was an unresponsive nociceptor, upregulate receptors that respond to different characterizations of pain --> active (silent becomes awake nociceptor) phenotype switching: have non-nociceptor afferent that suddenly starts to express nociceptor like properties in such a way that it will become like a fake nociceptor
46
LO12: What do nociceptors exist as?
FREE NERVE ENDINGS!! Axons of these neurons tend to have slowly conducting unmyelinated (C fibers) or thinly myelinated (Adelta fibers) axons with peripheral terminals not associated with specific structures or cell types
47
What are the types of characterization of free nerve endings?
Peptidergic- express neuropeptides (SP and CGRP) and are responsibe to nerve growth factor Non-peptidegeric = dont make peptides; responsive to GDNF
48
What is most of your viscera innervated by? How is chronic visceral pain produced?
Peptidegergic neurons responsive to NGF upregulation in pain as consequence of inflammation; expand nociceptor--> chronic visceral pain
49
Half of cutaneous afferents are innervated by what type of free nerve ending? What is associated?
non-peptidergic (respond to GDNF) Diabetic Neuropathy
50
*What do free nerve endings lack?
specialized receptor cells or encapsulations
51
What are the main TRP receptors? and what do they sense?
Sense noxious stimuli TRPV1, TRPA1, TRPM8
52
What are TRP receptors permeable to?
Ligand-gated non-selective cation channel permeable to Ca2+, Na+, and/or K+
53
What is TRPV1 associated with and what binds to the channel?
chili peppers!! Capsaicin binds it and chemical structure opens up, allowing Ca2+ to flow through--> pain
54
What is TRPM8 activated by?
activated my menthol
55
What is TRPA1 activated by?
allyl isothiocyanate (things find in environment but with enough of it--> pain) maybe garlic
56
What else can open TRP channels? Which ones?
temperature!! TRPVs are more responsive to hot temperatures (physically opens up)- themoreceptors: transmit temperature and pain info TRPAs are more activated by extreme cold
57
What are other signaling modalities of sensing noxious stimuli?
sodium channel (mutation- no pain or very extreme pain) ATP (p channels) H+ (ASIC channels) SP & CGRP- can circle back around and activate nociceptor again Histamine Kinins (bradykinin)
58
LO13: What do c fibers release?
EAA (Asp and Glut) and SP/CGRP
59
LO13: What do Adelta fibers release?
EAA only
60
What do EAAs bind?
non-NMDA receptors (e.g. AMPA)
61
LO13: How are nociceptors modulated?
by descending systems and interneurons in the dorsal horn
62
LO17: What is the gate control theory of pain?
(A) have C fiber coming in to dorsal horn of spinal cord (primary afferent comes in and synapses on secondary neuron which then goes up to brain); inhibitory interneuron hangs out and squirts inhibitory NT on secondary neuron (gate= closed) (B)With strong pain- two factor (activation and loss of gate) C fiber stops inhibition of pathway, allowing strong signal to be sent (C)Rub elbow- adding mechanoreceptor activity (light touch/pressure) through non-nociceptor (AB fiber) and have competition, little bit inhibitory and little positive signal; reduces sensation of pain
63
LO16: what are the descending influences on spinal cord transmission?
local system- gate control theory of pain (bump elbow and rubbing that spot) descending inhibition (dampen input on way to cortex)
64
LO16: What is descending inhibition pathway?
1. Periaqueductal gray are activated by opiates, EAA, and cannabinoids 2. send projections to locus coeruleus (NE) and raphe nucleus (5HT) 3. NE and 5HT released into dorsal horn and activate inhibitory interneurons 4. Local inhib. interneurons release opiates (enkephalin, etc.) 5. opiates activate mu receptors on pre-synaptic and postsynaptic terminals of C-fiber 6. results in reduction of SP from c-fiber and reduces nociception
65
LO16: What are the two ways descending inhibition can occur by serotonergic and noradrenergic neurons?
A. Can either directly inhibit the second order neuron, releasing something that inhibit it B. Or..Create intermediate interneuronthat would utilize opiates (enkephalens)- pain control chemicals in brain
66
LO16: Does the gate control theory explain everything?
NO peripheral signals central more from descending inhibition
67
What is an important molecule that is released during inflammatory states and can directly activate nociceptors?
BRADYKININ more= more NGF= more activity= more pain
68
LO15: What is cortical processing of nociceptive units? what is it important in?
most of nociception processed in the INSULAR CORTEX--> particularly of interpretation of nociception important in: integrating all signals related to pain!!!
69
LO15: What does damage to the insular cortex cause?
ASYMBOLIA- sensation of pain without emotional presence
70
What are other aspects of pain and what is important in it?
emotional component- amygdala visceral input with autonomic nerves- hypothalamus and medulla (physiological changes with visceral pain)
71
LO17: What are the mechanisms producing cutaneous pain? characterization?
sensitive to THERMAL pain, mechanical pain, and chemical pain sharp(fast) or dull/achy/throbbing (slow)
72
LO17: What are the mechanisms producing joint/bone deep pain? characterization?
mechanical and chemical usually dull and achy; assoc. with muscle spasm
73
LO17: What are the mechanisms producing muscle pain? characterization?
mechanical and sometimes chemical both fast and slow pain
74
LO17: What are the mechanisms producing visceral pain?
MECHANICAL (sensitive to stretch and stretch) and chemical poor localization, very sensitive to stretch; referred pain
75
LO18: What is referred pain?
brain requires some experience to localize pain, visceral pain is not experienced often in enough in early development to train brain to localize it afferents converge in dorsal horn!! hard to differentiate where problem arises antidromic signaling further diffuses visceral pain across multiple organs
76
What are common sites of referred pain from viscera?
esophagus, heart, urinary/bladder, left ureter, right prostate

Neuro test 2 (15 decks)

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