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NEUR 301 > Touch, Pain, Itch: Module 3.3 - 3.5 > Flashcards

Touch, Pain, Itch: Module 3.3 - 3.5 Flashcards

1
Q

What are the two types of touch?

A
  1. Active Touch
  2. Passive touch
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2
Q

What is active touch?

A

Top Down Process - You Initiate; CNS already recognizes and is aware of the same feeling; brain first.

During active touch, somatosenesory information depicts the physical properties of objects as well as the motor action sof the hand and arm, and their relation to task goals.

You move your hand

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3
Q

What is Passive Touch

A

Bottom Up Process - No preperation.

During passive touch, the subject reacts to external stimuli specifid bu the experimeter, clinican, someone else. The stimulus iscontrolled bu the someone else, and the subject needs to analyze all of the transmitted somatosensory information and select specific features part by the task instructions.

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4
Q

How many receptors provide touch sensation in the human hand?

A

4

Touch is a combined result of all of them.

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5
Q

What are the two types of axons tha innervate the 4 mechanoreceptors of the hand?

A
  1. SA (Slow Adapting)- Respond to steady skin indentation with a sustained discharge.
  2. RA (Rapid Adapting) - Fibers stop firing when indentation becomes stationary.
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6
Q

What are the 4 types of mechanoreceptors of the hand?

A
Meissner and Merkl - Have the most innervation and close to top of the skin. Charts: RA, SA, RA, SA
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7
Q

What are the characteristics of the 4 Mechanoreceptors of the hand?

A
Pay attention to Types, Best Stimulus, Response to Sustained Indentation.
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8
Q

Explain the organization of receptors in glabrous skin.

A
Receptors are innerated by large-diameter AB myelinated fibers. Fibers branch at their terminals to innervate several receptor organs. For Pacinian and Ruffini Corpuscles, fibers innervate only one receptor organ.
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9
Q

What are receptive fields?

A

Limited area in which mechanoreceptros convey sensory information.

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10
Q

Explain the difference between the receptive fields of Type 1 and Type 2 fibers.

A

Type 1 fibers have small, highly localized receptive fields withmultiple spots of high sensitivity that reflect the branching patterns of their axon terminals in the skin. An RA1 axon typically innervates 10-20 Meissner corpuscles, while an SA1fiber innervates approximately 20 Merkel cells.

Type 2 fibers innervating the deep layers of skin are connected to only a single Pacinian corpuscle or Ruffini ending. As these receptors are large, they collect information from a broader area of skin. Their receptive fields typically contain a single “hot spot” where sensitivity to touch is
greatest; this point is located directly above the receptor.

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11
Q

What place on the hand has the keenest sensitivity?

A

The distal pad of the index finger.

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12
Q

How do they use receptive fields for braille reading?

A

Dots spaced 3 mm apart, which is farther apart than the receptive field diameter of an SA1(Merkel) Fiber.

Also use RA1 however SA1 is the most.

Fires a burst when dot is in the field and is silent when dot leaves.

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13
Q

What do SA fibers actually sense and what properties of an object can this tell us?

A

SA1 and SA2 signal skin deformation and pressure.

Sensitive to edges, corners, points, and curvature, compliance, shape, size, surface texture.

We percieve an object as hard if it indents the skin and soft if we deform the object.

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14
Q

What specific deformation to SA2 fibers innervating Ruffini ending respond to?

A

Stretching of the Skin

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15
Q

What do RA fibers actually sense?

A

Sense Motion and Vibration.

Vibration sense is a useful measurement of dynamic sensitivity to touch.

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16
Q

What is the most sensitive mechano-receptor in the somatosensory system and best sensitive to vibratory simuli?

A

RA2 Pacinian Corpuscle

Can activate SA1 and RA1 but weaker. RA2 responsive to high freq 30-500hz vibrtions.
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17
Q

What is the best studied touch receptor organ?

A

Merkel Cell

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18
Q

Where do merkel cells usually cluster?

A

Cluster in swellings of hairy skins (touch domes).

Near the center of the fingerprint ridges in glabrous skin.

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19
Q

What are Markel cell-neutrie complexes?

A

Sensory epithelial cells innervated by large diameter AB sensory axons.

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20
Q

Explain signal transduction in regards to touch of Merkel Cells.

A
Touch triggers a train of action potentials (frequency proportional to the velocity and amplitude of stimulus) Piezo2 is expressed in both, Merkel cell and the SA1. Diagram-Sensory Transduction: Piezo2 channels in sensory neuron open uponstimulation (1) generating the initial dynamic response to touch (2). Skin deformation simultaneously activates Piezo2 channels in the Merkel cell (3), depolarizing activates Cav (4), and release neurotransmitter continuously (5). Binding of the neurotransmitter further depolarizes the SA1 neurite, producing sustain
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21
Q

What are the two examples of merkel cell recordings?

A
Piezo 2 Receptor Current goes through 0 because it is Cation Non-Selective
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22
Q

What are the 2 Piezo protein isoforms?

A
  1. Piezo1: Found primarily in nonneural tissue, such as epithelia in blood vessels the kidneym and bladderm and in RBCs.
  2. Piezo2: Expressed in Mechanosensory DRG and tregeminal neurons tha tmediate the senses of touch and proprioception and in vagal afferents innervating smooth muscle of the lung, where they sense lung stretch.
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23
Q

Explain structural characteristics of the Piezo Protein family.

A

The Piezo protein family of transmembrane ion channels are molecular mediators of mechanoreception in mammals.

Piezo1 proteins are composed of approximately 2,500 amino acids, with at least 26 transmembrane α-helices.

The ion channel is a** trimer formed from three identical subunits**, with two pore-forming α-helices at the C-terminal end of each Piezo protein.

The N-terminals of the subunits form a propeller-like structure, which is thought to be involved in coupling mechanical stimuli to channelgating.

They form cation non-selective channels

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24
Q

What conditions can arise from loss of Piezo 2?

A
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25
Q

What are the differences in activation between Piezo1 and Piezo2?

A

Piezo1: Activated by both negative and postiive pressure. - Due to being in Gut in which pressure can go both ways.

Piezo 2: Activated by only postive pressure. - Most important in Proprioception.

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26
Q

What is pain?

A
  • The ability ot detect noxious stimuli.
  • Is essential to an organisms survival and wellbeing.
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27
Q

What are the 2 types of pain?

A
  • Acute
  • Chronic - Pathological
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28
Q

What are the 2 ways someone can have a change in pain perception?

A
  • Reduced Sensitivity (Leads to injury) (Can involve other tissues)
  • Increased sensitivity (Allodyna and hyperalgesia)

Reduced can lead to amputation in type 2 diabetes.

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29
Q

What is nociception?

A

The process by which intense thermal, mechanical, or chemical stimuli are detected by a subpopulation of peripheral nerve fibers, called nociceptors.

Refers to whole structures not specific receptors.

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30
Q

What are nociceptors and what are the 3 types?

A

Nociceptors: Free nerve endings of primary sensory neurons.
**
3 Types:**

1) Thermal nociceptors: activated by temp. > 45°C or < than 5°C. They
include myelinated Aδ fibers (5-30 m/s) and unmyelinated C-fibers (1 m/s).

2) Mechanical nociceptors: activated by intense pressure applied to the skin.
Also endings of myelinated Aδ axons.

3) Polymodal nociceptors: activated by high-intensity mechanical, chemical,
or thermal (both hot and cold) stimuli. Predominantly of unmyelinated C
fibers

These three classes of nociceptors are widely distributed in skin and deep
tissues and are often co-activated.

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31
Q

How are the different type of nerve fibers are involved with pain and nociceptive transmission?

A

No Pain (Myelinated)
Aa Fibers: Proprioception
AB Fibers: Touch

Pain
Ad Fibers: Pain and Temp
C Fibers: Pain, Temp and Itch (Not Myelinated)

Example of Pain Transduction Second Pain is very Painful
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32
Q

Explain the different regions of the dorsal horn and what they recieve.

A
Red are Pain Lamina
33
Q

What are the 4 Ascending Nociceptive Pathways?

A
  1. Spinothalamic
  2. Spinoreticular Tracct
  3. Spinoparabrachial Tract
  4. Spinohypothalamic Tract
Amygdald - Reason why Pain is Emotional Spinohypothalamic Tract - Autonomic Response Both Pain Pathways Cross Spinal Cord right Away.
34
Q

Explain the Gate control theory of pain.

A

Theory states that the spinal cord has a gating mechanism that controls whether pain signals are sent to the brain or not.

Possible reason why rubbing the site of pain can alleviate the pain.

The projection neuron is excited by both (A and C fibres) classes of sensory neurons and inhibited by interneurons in the superficial dorsal horn. The two classes of sensory fibers also terminate on the inhibitory interneurons: - the C fibers inhibit the interneurons “opening the gate” - the Aβ fiber excite the interneurons “closing the gate”
35
Q

What is referred pain?

A

Is a condition in which pain from injury to a visceral tissue is percieved as originating from a region of the body surface.

Associated with large organs -> Possible adaptive advantage targeting extremeties to cause rest when internal organs are in pain.

36
Q

What is a possible explanation for referred pain?

A

The convergence of somatic and visceral nociceptive inputs onto lamina V neruons.

Why heart problems involve left arm pain.
37
Q

What are two common changes in pain perception?

A
  • Allodynia
  • Hyperalgesia
38
Q

What is Allodynia?

A

Pain in respoinse to stimuli that aare normally innocuous (not harmful).

Light storking sunburnt skin, movement of joints with arthritis.

39
Q

Whatis hyperalgesia?

A

An exaggerated response to noxious stimuli.

Persistent pain in absence of sensory stimulation.

40
Q

What are 2 types of chronic pain?

A
  1. Nociceptive pain
  2. Neuropathic Pain
41
Q

What causes Nociceptive Pain?

A

Activation of nociceptors in the skin or soft tissue in response to tissue injury. Occurs with inflammation.

Treated with NSAIDS or opiates.

42
Q

What causes Neuropathic Pain?

A

Results from direct injury to nerves in the PNS or CNS. Burning or Electric Sensation. (egL shingles, phantom limb pain)

Responds to NSAIDS not opiates.

43
Q

What is the primary NT released by Nociceptors and what are the cotransmitters released?

A

Primary: Glutamate

Cotransmitters: Neuropeptides - Substance P, CGRP, somatostatin, galanin.

Glutamate stored in small vesicles, NPeptides stored in dense core ones.

Substance P is released from the central terminals of nociceptive afferents in response to tissue injury or after intense stimulation of peripheral nerves. Although the physiological actions of glutamate and neuropeptides on dorsal horn neurons are different, these transmitters act coordinately to regulate the firing properties of dorsal horn neurons.
44
Q

Explain sensitization of peripheral nociceptors.

A

Damaged tissues release a cocktail of peptides and proteins. This cocktail decreases the threshold of nociceptor activation.

Local - Red area around injury is sensitized.

Bradykinin, Substance P, Nerve Growth Factor, ATP, Histamine, 5HT, etc.

45
Q

What is the main molecule contributing to sensitization?

A

Bradykinin (Active Pain-producing agent) - Activates Ad and C nociceptors.

Decreaes firing threshold.

46
Q

Explain How Neurogenic inflammation works.

A
Neurogenic inflammation: bradykinin and prostaglandins from insured tissues activate or sensitize nociceptors. Nociceptors release of substance P and CGRP. Substance P acts on mast cells, which release histamine. Histamine directly excites nociceptors. Substance P also produces plasma extravasation and edema, and CGRP produces dilation of peripheral blood vessels (red skin); the resultant inflammation causes additional liberation of bradykinin (further spreading).
47
Q

What is the mechanism in which Bradykinin works to increase sensitivity?

A

Modulates TRP Channels

Amplifies Heat TRP and inhibits Cold TRP.

Bradykinin (BK), which is released form tissues after injury, binds to G protein–coupled receptors on the surface of primary afferent neurons to activate phospholipase C (PLC), leading to the hydrolysis of membrane phosphatidylinositol bisphosphate (PIP 2), the production of inositol 1,4,5- trisphosphate (IP 3), and the release of Ca2+ from intracellular stores. Activation of protein kinase C (PKC) regulates TRP channel activity by phosphorylation. The TRPV1 channel is sensitized, leading to channel opening and Ca2+ influx.
48
Q

What is a major contributor to neuropathic pain due to nerve injury?

A

Central Sensitization

Can Decrease pain thesholds leading to allodynia and spontaneous pain.

49
Q

How does central sensitization work?

A

Repeated Exposure to noxious stimuli results in long term changes in the dorsal horn neurons.

Prolonged changes in dorsal horn neurons constitute a “memory” of C fiber input.

Involves C fibers, NMDA receptors, and need Neuropeptides

C fibers continuously transmit signals in response to prolonged or intense peripheral injury (e.g., inflammation or tissue damage). These sustained inputs release neuropeptides and excitatory neurotransmitters, which drive changes in the CNS, particularly in the dorsal horn of the spinal cord. Substance P: Released from presynaptic terminals of C fibers. Binds to neurokinin-1 (NK-1) receptors on postsynaptic neurons. Enhances neuronal excitability and promotes the persistent activation of second-order neurons. Glutamate: Released in excess during sustained C fiber activation. Activates AMPA receptors for initial excitation and NMDA receptors for long-term potentiation (LTP). NMDA receptor activation leads to increased calcium influx, triggering synaptic plasticity and prolonged excitability in the spinal cord
50
Q

What is analgesia?

A

Insensibility to pain without loss of consciousness.

51
Q

What are some examples of opiod receptors?

A

Mu, Delta, Kappa, Orphanin

52
Q

What are some endogenous opioids?

A

Enkephalins, B-Endorphins, Dynorphins

53
Q

Why is morphine use as an analgesic?

A

Morphine controls pain by activating opioid receptors and by mimicking the actions of endogenous opioid peptides.

54
Q

What are the 2 effects of opiodids on nociceptor signal transmission?

A
  • Presynaptic (DRG) - Reducing Ca entry and NT release.
  • Postsynaptic (projection neuron) - Increase K conductance, hyperpolariztion and increasing activation threshold (hyposensitivity).
55
Q

What is the mechanism in which opioids work?

A
The dorsal horn contains interneurons that express enkephalin and dynorphin, and the terminals of these neurons lie close to synapses formed by nociceptive sensory neurons and dorsal horn neurons. Morphine acts activates opioid receptors on Presynaptic and Postsynaptic Neurons as well as also activates release of Endogenous opioids from interneurons.
56
Q

What is an itch and what it its purpose?

A

Acute Pruitus (itch) serves as an alarm signal to protect the body against potentially harmful environamental threats (parasites, noxious plants or other irritants.

The scratch reponse helps to remove these irritants from the skin and reduces the itch sensation.

57
Q

What are 2 related sensations, what type of neurons are they detected by, what are there behavioral respones?

A

Pain and Itch

Detected: By small diamter DRG Neurons.

2 Behavioral Responses

Itch - Elicits scratching to remove irritants
Pain - Generates a withdrawal response to avoid tissue damage.

58
Q

Can pain supress itch?

A

Yes

Pain generated by scratching relieves itchy sensation.

59
Q

Can Itch Suppress Pain?

A

Rarely

60
Q

Can Itch Responsive Neurons in the DRG and Spinal Cord be activated by Pain?

A

Yes

61
Q

What is the inensity theory?

A

Poly-modal sensory neurons respond to both pain and itch stimuli.

Strong stimuli generate pain where weaker generate itch.

However… weaker painful stimuli or stronger itchy
stimuli fail to turn into a different sensation, thus
raising questions about the intensity theory.

62
Q

What is the selectivity theory?

A

Itchy stimuli specifically activate itch selective neurons to generate itch sensation.

Painful stimuli activate both itch and a larger nociceptive population whose activation inhibits itch to produce only pain sensation

63
Q

What places is itch confined to?

A

Skin, Ocular Conjuctiva, Mucosa

64
Q

What are itch specific peripheral sensory neurons called?

A

Pruiceptors

Sub group of nociceptive neurons.

65
Q

What discovery led itch to be a seperate biological and sensory process from pain?

A

The discovery of an itch-specific pathwag in the NS defined by gastrin-releasing peptide and its receptors.

66
Q

What axon types is involved in Nociception and Pruriception?

A

Ad and C fibers.

67
Q

What ascending pathway does itch take?

A

Same Pathway through the Spinothalamic Tract

Note: No emotional response.
68
Q

What is acute itch and what is its mechanism?

A

Acute pruritus (itch) serves as an alarm signal to protect the body against potentially harmful environmental threats.

Mainly mediated by histamine-responsive sensory neurons in the skin that are relatively insensitive to mechanical pain stimuli
but also respond to noxious chemicals such as capsaicin (TRPV1 agonist)

69
Q

What can chronic itch be caused by and what is the mechanism throught to be?

A

Seriously debilitating symptom accompanying
various cutaneous and systemic disorders but may also be caused by drugs such as the anti-malaria drug chloroquine.

Antihistamines do not improve some chronic itching, suggesting that it is mediated via histamine- independent pathways

70
Q

What is chronic itch frequently accompanied by?

A

Allokinesis and HyperKinesis

Involuntary Motion

71
Q

What are the 3 Pruriceptor classification and what are they activated by?

A

NP1: Activated specifically by β-alanine. NP1 expresses the B-alanine receptor MrgprD

NP2: Activated by chloroquine. NP2
expresses its receptor MrgprA3

NP3: Defined in part by its expression of the
receptor for IL-31 (IL-31RA)

72
Q

Explain the NP3 - Mediated Itch Pathway.

A
NP3 neurons express brain natriuretic peptide (BNP) which then activates the release of gastrin-releasing peptide (GRP) from interneurons in the spinal cord. GRP is a critical mediator of itch in the spinal cord by binding its receptor, GRPR, on spinal neurons, which then relay via projection neurons to the brain.
73
Q

What is the mechanism of histamine-dependant (Acute) itch?

A

Itch induced by intradermal injection of histamine or by procedures that release endogenous histamine activates a subset of TRPV1-expressing neurons that also contain the H1 histamine receptor; these itch sensations are blocked by
antihistamines.

It requires phosphorylation of TRPV1 (PKC

74
Q

What is the mechanism of histamine-independent (chronic) itch?

A
Histamine-independent itch appears to be mediated by C fiber DRGs that express TRPA1 channels. Itch sensations in this pathway are triggered by dry skin or by pruritogens that bind to members of the Mas-related G protein–coupled receptor (Mrgpr) family, such as the antimalarial drug chloroquine. Phosphorylation of TRPA1 by possibly PKC is required.
75
Q

What do TRPA1 receptors bind?

A

Bind pungent substances such as horeseradish, garlic, onions, allium expressing plants.

Produce pain or itch due to covalent modification of cysteines in TRPA1

76
Q

What are the 2 types of itch-selective nerves and what are the different receptors expressed on them.

A
  1. Histaminergic - H1R and H4R Receptor
  2. Nonhistaminergic - Variety of receptors responding to other pruritogens.
Note the location of TRPV1 and Nav 1.7 in both nerves.
77
Q

How can TRPa1 receptors mediate itch when they are also involved in sensing noxious cold temeratures?

A

Noxius cold is sensed when both TRPA1 and TRPM8 receptors are excited, but itch is perceived when TRPM8 receptors are silent/not present.

78
Q

Why do some TRPV1-expressing fibers mediate itch sensations rather than sensations of noxious heat?

A

Heat pain is sensed when TRPV1-, TRPV2-, and TRPV3-expressing fibers are co-activated, but itch may be perceived when only TRPV1- expressing fibers respond and TRPV2 and TRPV3 receptors are silent (or not present)

79
Q
A

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