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Neuro Exam 2 > Sensory Physiology > Flashcards

Sensory Physiology Flashcards

1
Q

What are peripheral neurons?

A

Nerves in the perphy: can be sensory (afferent) or motor (efferent)

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2
Q

Peripheral nerves are classified by two schemes.

A
  1. A, B C wave peripheral nerve: based on its contribution to a compound action potential from mixed nerves.
  2. AFFERENT FIBER characteristics: diameter, myeling thickness and conduction velocity (I, II, III and IV). Efferent fibers cannot be given these characteristics.
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3
Q

How is a peripheral nerves contribtion to a compound AP related to its characteristics.

A

• Conduction velocity determines a fiber’s contribution to the compound action potential. The compound AP and the conduction velocity are used to diagnose peripheral nerve disease.

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4
Q

What type of sensory (afferent) fiber types do we have?

A
  1. A: Aalpha, Abeta, Adelta
  2. C
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5
Q

SENSORY AFFERENTS

SENSORY AFFERENTS

SENSORY AFFERENTS

SENSORY AFFERENTS

SENSORY AFFERENTS

SENSORY AFFERENTS

A

Abeta (II); skin mechanoreceptors and secondary muscle spindles

Adelta (III); skin mechnoreceptors, thermoreceptors and nociceptors

C (IV): smallest diameter and the slowest; skin mechanoreceptors, thermoreceptors and nociceptors

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6
Q

Which sensory (afferent) fibers are our fastest and largest and where do they go to?

A

Aalpha; Ia and Ib; they go to primary muscle spindles, golgi tendon organ

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7
Q

Which sensory (afferent) fibers are our slowest and smallest and where do they go to?

A

C fibers (IV); go to skin mechanorecpetors, thermal receptors and nociceptors

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8
Q

Sensory receptors are will only respond to a certain modality.

Somatosensory receptors are _______

A

pseudounipolar

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9
Q

R_eceptor types vary a_cross sensory systems: they will perform the same function in different ways

But what do they all do?

A

They all convert the NRG that they’re sensitive to -> alter membrane potential

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10
Q

What is a generator potential?

A

A change in membrane potential that is seen when a stimulus is applied to a somatosensory receptor. When strong enough, it can cause a AP that can go t/o nervous system.

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11
Q

Convergence and divergence occurs where?

A

At receptors

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12
Q

Information from all sensory systems except the ______go through the ______ –> CTX.

A

olfactory

thalamus

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13
Q

How is sensory input arranged in the thalamus?

A

Thalamus has 1 single large nuclei for sensory input; but 2 nuclei (one for face and body) for somatosensory input. Here, the neurons that perform 1 function (touch) are separate from those that perform another function (propioception)

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14
Q

What is convergence?

A

2nd order neuron receives input from two different 1st order neurons

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15
Q

What is divergence?

A
  1. 1st order neurons have 2 branches that go to 2 different 2nd order neurons.
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16
Q

What is the difference between weak and strong stimuli?

A
  1. Weak strongly: a stimulus only activates only SOME branches of 1 sensory fiber or only activate 1 afferent neuron in a group of sensory units.
  2. Strong stimuli: stimulutes activates all branches of 1 sensory fiber or all afferent fibers in a group
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17
Q

How is the number of active receptors affected by the intensity of the stimulus?

A

increased intensity of the stimulus= INCREASE NUMBER OF ACTIVE RECEPTOORS

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18
Q

The number of active receptors increases with increased intensity of the stimulus. This allows for what?

A

This is how our senses can quantify small differences, allowing for very good discriminating ability

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19
Q

• Sensory receptors encode the intensity of the stimulus in _________

A

into amplitude of the receptor potential

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20
Q

When a stimulus persists unchanged for several minutes without a change in position or amplitude, what happens?

A

neural response diminishes and sensation is lost, resulting in receptor adaptation

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21
Q

The number of AP a stimulus produces depends on what?

A

strength of the stimulus

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22
Q

-Receptor adaptation uses two types of receptors: slowly adapting receptors and rapidly adapting receptors. What are the differences?

A

Slowly adapting receptors: receptors that respond to a prolonged, constant stimulation before it adapts.

Rapidly adapting receptors: receptors that respond to the begining and end of a stimulus and are only active if there is a change in intensity.

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23
Q

What does a slowly adapting receptor look like and give an example?

A

Tires fast at the begining, but continuelly fires for a prolonged period of time.

Ex. Myelinated fibers associated with smooth muscle of proximal airway

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24
Q

___________. are responsible for the sense of touch.

List them all

A

Mechanoreceptors (6) that respond to TOUCH

    1. Meissner corpsucles
    1. Pacinian corpsucles
    1. Ruffini endings
    1. Merkel cell
    1. Free nerve actings (tactile information)
    1. Hair follicle receptor
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25
Q

Identify the following as slowly adapting or fast adapting:

  1. Meissner corpsucles
  2. Pacinian corpsucles
  3. Ruffini endings
  4. Merkel cell
  5. Free nerve actings (tactile information)
  6. Hair follicle receptor
A

1. Meissner corpsucles-> RA

2. Pacinian corpsucles-> RA

3. Ruffini endings-> SA

4. Merkel cell-> SA

5. Free nerve actings (tactile information)-> SA (but these do tactile information)

6. Hair follicle receptor-> RA or SA

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26
Q

What type of information do the following convey?

  1. Meissner corpsucles
  2. Pacinian corpsucles
  3. Ruffini endings
  4. Merkel cell
  5. Free nerve actings (tactile information)
  6. Hair follicle receptor
A
  1. Meissner corpsucles-> tap and flutter (v sensitive- on fingers, lips)
  2. Pacinian corpsucles-> vibration
  3. Ruffini endings-> stretch of skin
  4. Merkel cell-> touch and pressure
  5. Free nerve actings (tactile information)-> tactile information
  6. Hair follicle receptor-> motion and direction
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27
Q

What is the average receptivefield size of the following?

  1. Meissner corpsucles
  2. Pacinian corpsucles
  3. Merkel cell
A
  • Meisners and merkel: small (more accurate)
  • Pacinian: large (less accurate)
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28
Q

what is a Receptive fields

A

Innervation of peripheral branches of ONE mechanorecptor on the skin.

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29
Q

REceptive fields allow us to test ______, which is what?

A

two point discrimination, which calculates spatial resolution for detailed structures

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30
Q

Does receptor adaptation = receptive field size?

A

no

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31
Q

• Tactile acuity is highest in _______________ (______receptive fields).

Tactile acuity is lowest on the___________ (______ receptive field)

A

• Tactile acuity is highest in lips and fingertips (smallest receptive fields).

Tactile acuity is lowest on the calf, back, thigh (largest receptive field)

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32
Q

how to conduct a receptive field test

A

put compass on two different receptive fields–> bring them close together until they can only feel 1 stimulus

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33
Q

Say we have a compasses (used to test 2-point discrimination) on two receptive fields on two different people.

Person A has many primary sensory neurons converging on a single secondary neuron; person B has few convergence occur. How will they differ.

A
  1. Two stimu;o compressing on two different receptive fields: if many primary sensory neurons converge on a single secondary neuron -> creates a secondary large receptive field -> thus, the brain will only sense 1 signal d/t convergence.
  2. In the other person, less conergence occurs, creating a smaller secondary receptor reptive field. Thus, two stimuli activate two different pathways and perceive as two different stimuli
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34
Q

Primary afferent neurotransmission is controlled by____________

A

pre and post-synpatic inhibitory mechanisms.

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35
Q

Primary afferent neurotransmission is controlled by pre- and postsynaptic inhibitory mechanisms.

Which exerts the most powerful form of inhibition and what is it?

A

Presynaptic inhibition is the strongest: causing a diminished excitatory signal.

  • 1.. Presynaptic inhibition occurs when one of the 1st order neuron releases GABA
    1. influx of Cl- into the axon
    1. Results in hyperpolarization
    1. Less Ca2+ enters cytosol
    1. Leads to less total NT release
    1. Allows us to better localize the signal by not activating neurons located laterally
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36
Q

Pre-synaptic inhibition results in what?

A

reduced NT release from the pre-synaptic terminal, improving the brain to LOCALIZE THE SIGNAL and figure out what we are feeling because we dont want sensory overload.

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37
Q

What is another type of pre-synaptic inhibition

A

2nd order neuron that was primarilty impacteed will have branches that inhibit fibers of lateral axons ->

38
Q

To better enhace the perception of a stimulus _________ can repeat all the way to the cortex, further narrowing the signal.

A

convergence

divergence

presynpatic inhibition

39
Q

What is cortical processing?

A
  1. Initial processing of the signal
  2. Integration of the initial processing into larger schemes
  3. Emotional response to the processing
40
Q

Are somatotopic maps (homunulus) fixed?

A

No: Continual input to one part of the somatosensory system map can increase area of cortex develoted to it (practiving OMM).

Restricting input can decrease area of CTX devleoted to it (amputation)

41
Q

How is the cortex arranged?

Main input for thalamus?

Main output?

A
  • 6 layers with projections in, ascending and descening projections out.
  • 3 and 4 are enlarged in the primary sensory cortex beause they are the primary input layer of the thalamus.
  • Main output layer: pyramidal cells
42
Q

Are our somatosensory CTX and PMC connected?

A

Yes via corticoconnection

43
Q

Our cortex has 6 layers. Within these 6 layers, what is the arrangement?

A
  1. Neurons are stacked above and below each other into columns, each with one sensory modality in one part of the body.
  2. Adjacent columns get sensory information from same part of body but different sensory modality.
44
Q

At layer______ where the input signals first enter the primary sensory CTX, the columns function almost entirely separate from each other.

At other levels of the columns, interactions occur that znalze of meaning of these signals

A

LAYER 4 via thalamus

45
Q

Sensory cortex includes:

A

1. Primary somatosensory cortex (S1): BA 3,1, 2

2. Secondary somatosensory CTX (S2)

3. Patieto-temporal-occiptal association cortex

46
Q

1. Primary somatosensory cortex (S1):

Receives what information:

Role:

A
  • 1st stop for most cutaneous senses (we get touched-> primary somatosensory is the first stop)
  • It integrages information about position (propioception) and size, shape discrimination.
47
Q

Secondary somatosensory cortex (S2)

Located:

Receives input from:

Role:

A
  • Located: wall of sylvian fissure
  • receives input from: S1
  • compares between different objects (tennis ball and baseball) and tactile sensation via touch and detrmines whether someone should become a memory.
48
Q

What is the PTO?

A

Parieto -temporal -occipital association cortex that receives input from multiple sensory areas and is responsible for high level interpretation of sensory input.

49
Q

What sensory CTX helps us:

  1. Analyze spatioal coordinates of seldf
  2. name objects
A

PTO

50
Q

How do we better engage in focusing events, such as reading?

A

Primary somatosensory CTX is going to descend fibers to subcortical areas, like the thalamas

51
Q

What allows us to process multiple sensation at once (be able to smell and talk at the same time)?

A

Cortico-cortical projection

Links primary and association areas of the sensory cortex, allowing us to process multiple sensation at the same time. These connections can be contralateral or ipsilateral via the CC.

52
Q

What cortical tracts help us to control the intensity of sensory infomration via inhibition?

bc we want to prevent sensory overload!

A

Corticofugal signals: CTX -> lower relay stations in the thalamus, medulla or SC t

53
Q

what is the Doctrine of specific nerve energies

A

No matter where along the afferent pathway is stimulated, the sensation that will occur is determined by the nature of the sensory receptor in the periphery connected to that pathway.

no matter where along the afferent pathway you stimulate, the sensation that is convey that will be determined by the receptor of that pathway: light touch -> light touch -> l..

54
Q

Law of projections

A

any stimulation along that path will cause sensation at the origin of sensation:

touch with right thumb, feel with right thumb

55
Q

Articulate the difference between nociception and pain.

A

Pain: unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

Nociceptin: the process of encoding noxious stimuli, a stimulus that can cause damage or threaten damage.

56
Q

Nociception can cause what?

A

1. Autonomic consequences ( high BP)

2. Behavorial consquences (withdraw reflex)

You dont necessarility have to feel pain.

57
Q

What fibers transmit pain?

A
  1. A(delta) fibers: fast and sharp pain
  2. C fibers: allows prolonged, slow pain bc not myelinated
58
Q

If pain activates both A(delta) and C fibers, what happens?

A

Sharp pain at first, then prolonged pain.

Ex: cut yourself really bad and the pain that persists

59
Q

What locations can we feel pain from? What transmits the pain?

A
  1. Somatic or cutaneous pain, muscle pain, deep pain or visceral pain
  2. Will be transmited via nociceptors
60
Q

What is a nociceptor?

A

Sensory receptor of the peripheral somatosensory NS with a high thresthold that can transduce noxious stimuli

61
Q

Types of pain?

A

1. Thermal

2. Chemical

3. MEchanical

62
Q

Can nociceptors respnd to more than one modality or are they specific for one?

A

They can be polymodal (responding to more than one modality)

63
Q

Silent nociceptors are related to the phenomenon of phenotype switching.

What does this mean?

A

Silent nociceptors Although each nociceptor can have a variety of possible threshold levels, some do not respond at all to chemical, thermal or mechanical stimuli unless injury actually has occurred. These are typically referred to as silent or sleeping nociceptors since their response comes only on the onset of inflammation to the surrounding tissue by altering genes

Phenotype switching: a non-nociceptor that changes phenotype to express nocicpeptor like properties.

64
Q

Describe the axons of neurons that trasnmit pain.

A

Axons are slowly conducting, unmyelinated (C fibers) or thinly myelinated (Aδ fibers) axons with peripheral terminals that d_o not have a speicifc structure or cell type_ (free nerve endings)

65
Q

Do free nerve endings bind to specific receptors?

A

No. they lack specialized receptors

66
Q

Do free nerve endings have encapsulations?

A

no

67
Q

What are our two types of FNE?

A

1. Peptidergic FNE express substance P and CGRP. They grow in response to nerve growth fact (NGF). They make up most visceral afferents and 1/2 of cutaneous afferent (chronic inflammation and visceral pain).

2. Nonpeptidergic do not have neuropeptides. Grow in responds to GDNF (glial derived neurotrophic fact). MAke up few visceral afferents and 1/2 cutaneous afferents (role in diabetic neuropthathy)

68
Q

What are TRP receptors?

A

TRP receptors are ligand- gated non-selective ion channel that are permeable to Ca2***, Na+ or K. They are another way to detect pain and TEMPERATURE

69
Q

What are important family of TRP receptors and what bind to them

A
  1. TRPV1 -> bind capsaicin (peppers)
  2. TRPA1-> allyl isothiocyanate (radishes, mustard powder, garlic)
  3. TRPM8- > bind mint (menthol
70
Q

Which TRP receptors respond to extreme heat and cold?

A

Extreme heat -> TRPV1

Extreme cold -> TRPA1

71
Q

What are other ways to sense noxious stimuli (6)?

A

1. Na 1.7 Na+ channel

2. ATP via P2X

3 . H+ via ASIC (detects acids)

4. SP and CGRP

5. Histamine

6. Kinins (bradykinin.

72
Q

C fibers release what?

A
  1. EAA -> which binds to non-NMDA receptors
  2. SP/CGRP
73
Q

Adelta fibers release

A
  1. EAA, which binds to non-NMDA receptors
74
Q

Describe the descending influences on spinal cord transmission of nociceptive inputs and explain their clinical relevance.

modulate pain?

A
  • Nociceptors are influenced by descending systems and interneurons in the descending horn. Descending inhibition can dampen input on its way to the CTX.
  • Local systems, such as the gate control theory of pain predicts that “rubbing the spot that hurts eases pain
75
Q

According to the gate theory of control of pain:

what happens when there is no pain, sharp pain, and can this pain be modulated?

A

Gate theory of control :we can modulate pain by input of simultaneous somatosensory information

  1. WHEN NO PAIN (input from C fibers); our GATE IS CLOSED: our t_onically active inhibitory interneuron_ supresses the pain pathway -> CTX.
  2. Strong pain: C fibers inhibit the inhibitory interneuron-> GATE OPENS-> allowing a strong painful stimulus -> brain
76
Q

According to the gate theory of control of pain:

what happens when there is no pain, sharp pain, and can this pain be modulated (GATE CONTROL THEORY)?

A
  • GATE CONTROL THEORY: we can modulate pain by input of simultaneous somatosensory information
    1. . Rubbing an area of affected skin activates the A β fiber
    1. Branches in the dorsal horn and synapses on an inhibitory interneuron
    1. Releases EAA.
    1. The activated interneuron releases glycine and inhibits the secondary sensory neuron of the nociceptive pathway -> decreasing pain
77
Q

What is the descending inhibition pathway?

A

Descending inhibition: dampens input on its way to the cortex

    1. Opiates, EAA, and cannabinoids activate PAG
    1. Descending projections travel to: Locus Coeruleus (NE) and Raphe nucleus (Serotonin)
    1. 5HT and NE released into dorsal horn
      * activate inhibitory interneurons (or they can inhibit 2nd order neuron)
    1. Local inhibitory interneurons release opiates (like enkephalin)
    1. Opiates activate mu receptors on pre-synaptic (and post-syanaptic) terminals of a C-fiber.
    1. Results in reduction of SP from the C-fiber and reduces nociception
78
Q

Descending serotonergic and noradrenergic neurons can do two things:

A
  1. Activate local inhibitory interneuroons-> release opiates
  2. Inhibit 2nd order neurons
79
Q

Gate control theory is responsible for ______ signals

Descending inhibition is responsible for _______ signals.

Thus, gate control theory DOES/DOES NOT explain everything.

A

Gate control: peripheral signals

Descending inhibition: central signals

does not

80
Q

What exaplins chronic pain and pain sensitization?

A
  1. Peripheral signals
  2. Central signals
  3. and higher brain centers
81
Q

What is neurogenic pain/inflammation disorders?

A

Sub-threshold pain caused by molecular levels of inflamation (not necessary seen on microscope) caused by inflammatory mediators, such as bradykinin that is relased during inflammation.

-> + nociceptors and + NGF , which activates more nocicpetors and + active peptidergic FNE

82
Q

S1 and S2 ______ receive input from nociceptors and play a role in localization of pain

A

DO

83
Q

Where is most nocicpeition information interpreted and processed?

A

• Insular cortex integrates all signals related to pain and processes/interprets the nociception.

84
Q

Whhat happens if we damage the insula?

A

Asymbolia-> pain is experienced, without the unpleasant sensation. Bc insula is what receives pain information and then INTERPRETS it.

EX. people who love pain ;) and laugh.

85
Q

Lesions in any single area alters what aspect of pain?

A

EXPERIENCE of pain, but it does not completely abolish it: for example, amygdala is important to the EMOTIONAL component of pain.

86
Q

What is responsible for integrating physiological changes that are associated with visceral pain?

A

Visceral input travels with autonomic nerves -> hypothalamus and medulla; where integration occurs

87
Q

Compare and contrast the mechanisms producing cutaneous, deep, muscle, visceral pain, and referred pain.

A
  1. Cutaneous: thermal, mechanical (cut, pinch), chemical
  2. Joints (deep): mechanical (torsion) and chemical (inflammatory mediators)
  3. Muscle: mechanical (blunt force) and chemical (inflammatory mediators)
  4. Viscera: mechanical (distension, traction of mesentary) and chemical
88
Q

Describe cutaneous pain and deep pain (to ligaments, periosteum, bone)

A
  1. Cuteneous pain: can be fast (sharp) and slow pain (dull and achy)
  2. Deep pain: usually dull and achy (muscle spasm)
89
Q

Describe muscle pain and visceral pain to internal organs

A
  1. Muscle pain: both fast pain and slow pain
  2. Visceral pain: poorly localized and VERY sensitive to stretch. It is assocated with referred pain
90
Q

Why do we get referred pain?

A
  1. Brain requires some experience to localize pain, visceral pain is not experienced often enough in early development to “train” the brain to localize it, causing referred pain.
  2. Nociceptors can innervate different parts of the body, but they converge on the same 2nd order neuron neuron in the dorsal horn. Ex. 2 different nociceptors detect pain: one from skin and one from intestines-> but they all converge in dorsal horn.
91
Q

What is a nociceptor?

A

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain. If the brain perceives the threat as credible, it creates the sensation of pain to direct attention to the body part, so the threat can hopefully be mitigated; this process is called nociception.

This is why noception alters our physioogical characteristics AND it alters behavir (withdrawlal reflexor)

Neuro Exam 2 (12 decks)

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