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Neuro > Somatosensory Physiology N19 > Flashcards

Somatosensory Physiology N19 Flashcards

1
Q

Sensory Transduction

A

process by which a stimulus is transformed into an electrical response

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2
Q

Sensory unit

A

one afferent peripheral process with all of its receptor endings and receptors

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3
Q

Receptors can be either

A

specialized endings of afferent neurons or separate receptor cells that signal afferent neurons via chemical messengers

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4
Q

Stimulus generates a

A

graded potential, or receptor potential, in the nerve generating a local current

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5
Q

Threshold in an afferent neuron

A

If threshold is reached, an AP travels to the CNS

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6
Q

Increase in graded potential magnitude generates

A

an increase in AP frequency and an increase in neurotransmitters released at the CNS synapse

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7
Q

Increase in graded potential magnitude does not change AP’s _____

A

magnitude

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8
Q

Factors that change the receptor potential magnitude

A

stimulus strength, rate of change of stimulus strength, temporal summation, and adaptation

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9
Q

Adaptation refers to

A

a change in receptor sensitivity due to constant stimuli, resulting in decreased AP frequency despite stimuli

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10
Q

Coding

A

conversion of stimulus energy into a signal that conveys relevant sensory information

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11
Q

Stimulus characteristics

A

location, type of energy, intensity of energy

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12
Q

Location of stimulus is determined by

A

which neuron is activated, each neuron terminates in a specific region of the CNS

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13
Q

Stimulus modality

A

type of sensory receptor a stimulus activates plays the primary role in coding

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14
Q

Mechanoreceptors

A

respond to mechanical stimuli (bending of hair, dee pressure, vibrations, stretch, and superficial touch)

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15
Q

Thermoreceptors

A

sensitive to temperature (cold: 10-38C, warm: 32-45C)

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16
Q

Thermal nociceptors

A

sensitive to cold pain or hot pain

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17
Q

Photoreceptors

A

respond to light of a particular wavelength

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18
Q

Chemoreceptors

A

respond to the binding of particular chemicals to the receptive membrane (internal: gas levels in blood; external: tastebuds on tongue)

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19
Q

Nociceptors

A

respond to stimuli that cause pain (excessive mechanical deformation, excessive temperatures, chemicals) free nerve endings

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20
Q

Adequate Stimulus

A

type of energy to which a particular receptor responds (very sensitive to specific energy form)

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21
Q

Sensory stimulation vs sensation

A

electrical stimulation of a “cold” primary afferent neuron may be perceived as a cold sensation, even though the “cold” thermoreceptor was not stimulated

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22
Q

Frequency Coding

A

the intensity of the stimulus is coded by the frequency of APs (stronger stimulus = greater AP frequency)

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23
Q

Population Coding

A

Stronger stimulus = larger area of receptors activated

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24
Q

Threshold

A

lowest stimulus intensity that a subject can reliably detect (varies by context, experience, fatigue, BUT does not represent a change in the receptor)

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25
Q

What would be a situation where the threshold is decreased?

A

Anticipation

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26
Q

What would be a situation where the threshold is increased?

A

Childbirth, competitive sports

27
Q

Rapidly Adapting Receptors

A

Respond rapidly at onset/offset of stimulus, but fir slowly or stop during remainder of stimulus. (Important for transient or dynamic stimuli)

28
Q

Slowly Adapting Receptors

A

Maintain activation throughout stimulus, provide info on static qualities of a slow changing or prolonged event

29
Q

Presynaptic Inhibition

A

descending inhibitory controls exerted on primary afferent neurons

30
Q

Central control of afferent information

A

as the AP travels to the cerebral cortex, signals may be modified at synapses

31
Q

Sensory Information vs Sensation vs Perception

A

Sensory Information: any signal received by afferent sensory neurons
Sensation: sensory signals that reach CONSCIOUSNESS
Perception: our interpretation of the signal

32
Q

Sensation and Pereption occur after CNS modification

A

CNS may accentuate, modify, or filter sensory information, and perception is also based on previous experiences

33
Q

Algesia

A

sensitivity to pain

34
Q

analgesia

A

selective suppression of pain

35
Q

Pain

A

a sensory or emotional experience associated with real or potential injuries

36
Q

First (fast) pain

A

nociceptive pain, processing of an acute, well localized stimulus; PROTECTIVE SENSATION

37
Q

Second (slow) pain

A

prolonged noxious stimulus that outlasts the stimulus, associated with inflammation due to tissue damage (NSAIDS decrease 2nd pain)

38
Q

Third (Neuropathic) Pain

A

chronic, non-protective, and pathological pain due to damage of the nerves (electric, burning) that may invoke fear, depression, anxiety

39
Q

Phantom Limb pain

A

traumatic or surgical limb amputation may result in chronic pain due to nerve damage

40
Q

Causalgia

A

Complex regional pain syndrome may occur after damage to a peripheral nerve

41
Q

Sensory component of pain (what information is processed and where)

A

processed at the spinal cord and higher brain centers; type, location, intensity, duration of pain

42
Q

Nociception activation

A

not necessarily lead to pain sensation, perception is the product of the brain’s processing of the sensory input

43
Q

Responses to painful stimuli include:

A

arousal, attention, somatic or autonomic reflexes, endocrine response, emotional change

44
Q

Nociceptor Anatomy

A

Free nerve ending in periphery –> release of glutamate and neuropeptide substance P in the spinal dorsal horn

45
Q

Thermal nociceptors

A

respond to extreme temperatures; A-delta small-diamter, thinly myelinated fibers

46
Q

Mechanical nociceptors

A

respond to intense pressure; A-delta small-diamter, thinly myelinated fibers

47
Q

Polymodal Nociceptors

A

respond to high intensity mechanical, chemical, or thermal stimuli; small diameter, non-myelinated slow-conductin C fibers

48
Q

First and Second pain response to injury

A

Pain is first rapidly realizes by “sharp” first pain A-delta fibers, while 2nd pain is mediated by C fibers that cause a dull ache

49
Q

Referred Pain

A

pain that is perceived to be coming from an area that is remote from the actual source of pain, due to convergence of somatic and visceral nociceptive input onto the same dorsal horn secondary neuron (indiscriminative of pain location)

50
Q

Sensitization of Nociceptors

A

after injury nociceptors may become sensitized (or activation of interneurons)

51
Q

Primary Hyperalgesia

A

noxious stimuli contacts injured site, the magnitude of pain increases due to sensitization and recruitment of additional nociceptors

52
Q

Secondary Hyperalgesia

A

nociceptors surrounding the injury site may become tender or sensitized and application of noxious stimulus may generate an excessive pain response

53
Q

Allodynia

A

non-noxious stimulus now evokes pain due to sensitization

54
Q

How does injury cause sensitization

A

injured tissues release bradykinin, serotonin, K+, and prostaglandins –> activate nociceptors–> local release of Substance P and Calcitonin gene related peptide (CRGP) –> causes mast cell degranulation –> histamine release –> directly exciting nociceptors

55
Q

Bradykinin is one of the most active pain producing agents because

A

it activates A-delta and C fibers and increases the release of prostaglandins

56
Q

How do NSAIDS block 2nd pain?

A

Block cyclooxygenase, which prevents the synthesis of prostaglandins

57
Q

Which substances are activators of afferent fibers?

A

K+, Serotonin, Bradykinin, Histamine

58
Q

Which substances cause sensitization of afferent fibers?

A

Prostaglandins, leukotrienes, and Substance P

59
Q

Inflammation and Substance P

A

dilation of peripheral vessels (heat, redness) and plasma extravasation (swelling); Substance P can cause all 3 symptoms and Substance P antagonists can block all 3 symptoms

60
Q

Hyperalgesia

A

caused by Substance P and CGRP mast cell activation –> histamine directly excites nearby nociceptors

61
Q

A-delta fibers release glutamate and

A

activate AMPA glutamate receptor subtype in dorsal horn = 1st pain

62
Q

C-fibers release glutamate and Substance P and

A

activate NMDA glutamate receipts subtype and NK-1 receptors = 2nd pain

63
Q

Central sensitization

A

chronic activation of C fibers and constant release of glutamate and Substance P = hyperexcitability and diffusion of neurotransmitters that activate nearby neurons

64
Q

Central sensitization decreases the threshold and produces:

A

hyperalgesia, allodynia, and neurpathic pain

Neuro (23 decks)

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