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302 - final > L 5 > Flashcards

L 5 Flashcards

1
Q

4 skin receptors

A

texture
pressure
vibration pain

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2
Q

what are 2 types of receptors

A

free nerve endings, hair cells

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3
Q

skin and body temperature

A

skin can control body temperature via messages from the hypothalamus. - change in [hormones] can constrict or dilate blood vessels and increase decrease sweating.

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4
Q

touch receptors effect what you buy - why?

cold and pain.

A

if you pick it up, tactile response gives you a sense of ownership over the object you touched. more likely to feel ownership and value the object if you touch it.
touch receptors can be influenced to feel cold or not, touch receptors can’t feel pain when watching pain.

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5
Q

what is congential analgesia

A

rare genetic disorder where individual is unable to feel pain.

    • shorter lifespan either bc don’t realize they need hurt.
    • objective, misinterpretation. inability to feel pain.
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6
Q

what is pain asymbolia

A

inability to feel negatve aspects of pain

  • not congenital, usually assoc w brain injury
  • feel location and intesnity of sensation, don’t interpret as negative or aversive.
  • subjective misinterpretation of pain
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7
Q

2 pain transducing free nerve endings

A

fast-acting a-delta fibers

slow c-fibers

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8
Q

fast-acting a-delta fibers

A

sharp pain
myelinated
goes away quickly

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9
Q

slower c-fibers

A

longer lasting
duller pain
non-myelinated

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10
Q

explain spinal reflex & pain

A

jerk hand from hot stove top. info received by spinal cord first, travels up to brain simultaneously to interpret as pain.

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11
Q

2 pain pathways/brain areas

A
  1. somatosensory cortex - mediates pain location and type
    - objective sensation of pain
    - interprets something is happening at this location
  2. hypothalamus/amygdala/frontal lobe - emotional motivation to escape the aversive stimulus
    - hypo = hormones
    - amygdala = emotions.
    - subjective interpretation of stimulus.
    = some or all affected in pain asymbolia
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12
Q

pain receptors that respond to heat

A

capcaicin: compounds in food bind to receptors in mouth = tell brain it’s physically hot.

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13
Q

immune cells & pain

A

immune cells make pain receptors more sensitive.

- release cytokines (Il-1/2) to make area of injury more sensitive to pain. - inform area it’s injured.

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14
Q

pain receptors and the bones/muscles/internals

A

internal pain may express as external pain = referred pain: sensory info converges on the same nerve cells in the spinal cord.
ex: heart attack. arm vs heart on same nerve, normally receive more info from the arm over heart, so the brain interprets any pain going thru there as arm pain

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15
Q

theory regarding modification of pain

A

gate-control theory of pain.

- signals from pain receptors can be inhibited.

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16
Q

two ways of inhibition of pain

A

skin receptors

periaqueductal grey

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17
Q

skin receptors & inhibition of pain
2 receptors on interneuron.
- top-down or bottom-up?

A
  1. a-delta neurons activate interneuron which inhibit the spinal afferent (less pain). a-delta activates spinal afferent directly as well (more pain).
  2. c-fibers inhibit interneuron. when active, inhibit interneuron so no inhibition on spinal afferent = more pain.
    bottom-up. sensation of pain changes experience.
    - treatment: use TENS : electrode in spinal cord. activates a-delta fibers to activate interneuron to inhibit the spinal afferent.
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18
Q

PAG and pain modification

A
  • inhibitory and excitatory fibers from the brain act on pain afferent in spinal cord.
  • endorphins = inhibitory action to decrease pain and firing of pain afferent = produced in pituitary - both ACTH and endorphins cleaved by same peptide = both produced when stress increased
  • PAG projections down to senses. excitatory = excite spinal afferent = increase pain. inhibitory = inhibit spinal afferent = less pain
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19
Q

pain & other modalities of touch

A
  • small nerve fibers: similar to c-fiber. inhibit interneuron to activate pain afferent = long lasting pain.
  • long nerve fibers (similar to a-delta). activate interneuron to inhibit pain afferent - decrease pain.
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20
Q

prolonged pain aka?

A

allodynia: feeling of pain in response to normal stimulus = reinterpret as painful.
may be due to immune cells bc they increase sensation of pain. overactive immune system + injury to increase it further = even more sensitive to pain & interpret normal as painful.

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21
Q

neuroma

A

tanglling of nerves.
- may occur bc immune cells release GH to grow nerve damaged tissue. nerves grow too quickly and get tangled up. neurons are hyperexcitable when tangled = regular touch interpreted as pain.

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22
Q

subjective interpretation of pain

  • trees and control
  • emotions and context
  • hypnotic analgesia
A

trees: correlation between window to outdoors and asking for less pain meds. when able to self-administer - less pain meds bc able to control.

emotion & context: pain is dependent on positive emotion and context. + context = less likely to feel pain. - emotion = more likely to feel pain.

hypnotic analgesia: trance-like state: can give suggestion to trance. hypnosis = highest pain reduction in pain - subjective & brain imagine. somatosensory and subjective areas of brain decrease activity when under hypnosis = less perception of pain.

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23
Q

stress induced analgesia

  • civilians vs soldiers
  • women vs men
  • rats on hot plate
A

c/s: when control for severity of injury. civilians request pain meds 80% of the time, whereas soldiers only request 30% of the time.
- m/w - stress task, physical stressor, stress task. women had stronger pain reduction than men. stress task, competitive stressor, stress task = men had greater reduction in pain. maybe men felt more invested that’s why they had betterresult.

  • rats = more stress induced analgesia
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24
Q

running

A

eustress

- takes about 30 mins for endorphins to build up to get runners high

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25
Q

biology of stress-induced analgesia
- function? feeling
opiate vs opioid

A

inhibitory, induce feelings of relaxation.
- opiate = plant (TT) opioid = synthetic.
bind to opiate receptors. mimic endorphins.

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26
Q

where are endorphins made?

A

endorphins made and released in areas of brain involved in pain perception.
- pit. PAG
inhibitory - decrease perception of pain

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27
Q

morphine - wanted to keep analgesic effect, decrease addictive properties

A

made heroin = more addictive

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28
Q

acupuncture
- animals and placebo
- stimulate release of ?
-

A

works on animals - must not be placebo.

- release of endorphin.

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29
Q

acupuncture subtraction experiment

A

– subtraction experiment: block opiate receptors with naloxone (competitive antagonist) - naloxone + acupuncture = no pain release

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30
Q

placebo effect of acupuncture

  • importance
  • seeing is believing
  • induced release
A

– placebo effects: placebo is important in mediating experienced pain. if subjectively reduced, its significant. seeing IV = stronger effect of pain reduction. if you think certain things will reduce pain, stress axis can induce endorphin release

31
Q

stress releases opioid - historical finding

A
  • beta-endorphin relased from pit. Guilleman: found stress hormone when finding whether hormones came from hypothal
32
Q

2 types of stress induced pain sensitivity

A

hyperalgesia

fibromyalgia

33
Q

what is hyperalgesia
- personality traits assoc?
what blocks stress-iduced hyperalgesia

A

increased sensitivity to pain

  • no definitive cause.
  • changes in subjective, emotional response can increase perception of pain.
  • neuroticism (higher functioning amygdala - increased emotional), anxiety (higher pain perception)
  • anti-anxiety block stress-induced hyperalgesia
34
Q

what is fibromyalgia

A

body-wide pain with no evidence of cause
- markedly reduced pain tolerance, feel pain from no stimulus.
more prevalent in high anxiety, high neuroticism - higher amygdala function and emotional interpretation of pain.
- lower glucocorticoid levels: not clear how it functions, but probably adrenal fatigue

35
Q

hyperalgesia - chronic stress

  • analgesia
A

pain continues and worsens.

- analgesia: adaptive for acute stressors. declines under chronic stress bc of exhaustive phase of stress.

36
Q

explicit vs implicit vs procedural memory

A

explicit: consciously or intentionally retrieve past experiences
declarative: factual.
implicit: past experiences influence later behaviour without conscious awareness of the memory. amnesics can develop implicit.
- procedural: gradual acquisition of skills through practice. motor cortex and cerebellum, not hippocampal.

37
Q

sapolsky’s trick

A

when losing in competition against someone, ask them to explicitly describe the task. interrupts implicit & procedural memory = makes action worse.

38
Q

hippocampal index

A

index for memories. brings together components of memory. in early formation, hippocampus links. each sensory experience stored in different areas of cortex.
- over time, memories no longer require hippocampal to connect. accumulate in one area of brain = hippocampal independent.

39
Q

HM could recall early childhood therefore

A

hippocampus not responsible for retrograde amnesia.

40
Q

glutamate

A

excitatory neurotransmitter. mostly cortex and hippocampus

41
Q

long term potentiation

A
  • communication across the synapse between neurons strengthens the connection, making further communication easier.
42
Q

what is strengthening the connection in terms of LTP

A

glu released in synapse - can act on AMPA and NMDA.
AMPA = ionotropic. glu binds, opens channel allows Na+ thru. Na+ in causes depol of post synaptic neuron = opens NMDA. depol causes MG2+ ion thats blocking channel to be repelled. Ca2+ and Na+ can then enter thru NMDA. opening of NMDA = increase Ca2+ - downstream effects like upregulate AMP receptor. less glu needed to depolarize to same amount as before upregulation of receptors therefore stronger response.

43
Q

difference btw AMPA and NMDA

A

AMPA: ionotropic. na in.
NMDA: mg block, Ca and na. ca has downstream effects like gene transcription for upregulation of AMPA receptors onto membrane. less glu needed to activate

44
Q

block LTP =?

A

block formation of new memories

45
Q

how to form new memories?

A

LTP, new synapses, new neurons.

46
Q

moderate short term stressors =?

A

enhance memory. recall and memory formation because of SNS release of A and NA

47
Q

exciting vs neutral story recall

A

one description of story = neutral. 2nd description exciting. exciting version was remembered better than neutral. increase in SNS benefitted memory.
- when add drug that blocks SNS activty (b-blocker) = no better recall.

48
Q

chronic stress and memory

A

explicit memory more affected than impllicit. - chronic stress acts on hippocampus.
- memory retrieval affected more than memory function.

49
Q

cushingoid dementia

A

cushing’s syndrome: tumor on adrenal gland results in excess secretion of glucocorticoids.
patient with cushingoid dementia - tested poorly in explicit mem.

50
Q

people treated with glucocorticoids - either synthetic or natural

A

explicit memory problems

- due to stress response. same severity of tumor elsewhere = less symptoms. less explicit mem problems.

51
Q

animal studies: hippocampal neurons, receptors

A

hippocampal neurons: glucocorticoids and SNS disrupt LTP. harder to from mem and recall.
hippocampal receptors: high affinity and low affinity to glucocorticoids. high [gluco] - high affinity activated= enhance LTP. in chronic stress - v high [gluco] = low affinity get bound = decrease LTP.

52
Q

animal studies: amygdala connects to hippocampus

A

destroy amygdala or connections: no effect of stress on memory - no better mem of exciting events.
- naturally amydgala stimulated by NA, releases gluco on hippocampus = memory enhancement.

53
Q

animal studies: atrophy of axons/dendrites from chronic stress

A

dendrites not as dense with stress. reduction in dendritic branching when high stress hormones for few weeks.

  • impair ability to recall.
    • can regrow if reduce stress hormones
54
Q

animal studies: neurogenesis

A

stress inhibits neurogeneis. prolonged glucocorticoids inhibit glucose delivery to hippocampus. neurons more likely to die.

55
Q

2 areas where adult neurogenesis occurs

A

olfactory system: pregnancy can cause new neurons = aversiveness to smell.
hippocampus.

56
Q

6 examples of human studies regarding smaller hippocampus due to stress hormones

A 
cushing's syndrome
major depression
repeated sleep loss
normal aging
neurological insults
PTSD
57
Q

cushing’s syndrome and hippocampus

A

cushingoid dementia - smaller hippocampus. not seen in other tumours. assoc w stress hormones being released from adrenal gland tumour.

58
Q

major depression and hippocampus

A

1/2 the ppl with depression have elevated glucocort levels. this is correlated to smaller hippocampus.

59
Q

aging - different social views. changes w age

A

societies may view old as - or +

  • social networks decrease with age. fewer friends, but quality improves.
  • cognitive skills - older ppl are better at using facts rather than just memorizing
60
Q

define aging

A

the progressive loss of the ability to deal with stress.

61
Q

ex of not activating enough stress response

  • chronic stress & addisons
  • heart
  • IQ scores
A

chronic stress & Addison’s disease = not activating at cellular level; DNA repair doesn’t function as well.

  • heart: cardio system doesnt respond as well when older vs when younger. older won’t get same maximal heart rate as younger even without cardio damage
  • IQ: add time stressor, everyone does worse. but older had significantly worse performance.
62
Q

ways in which body isnt responding well to a stressor

- 2 effects

A
  • not activating stress response
  • overactivating stress response
    effect: bones, hippocampal neurons
63
Q

ex of overactivating stress response

A

longer to turn off once initiated = higher baseline of stress hormones.
normal response = low baseline, shoot up quickly, stay high during stressor and decline to baseline quite quickly.
improper function: higher baseline, longer at eah stel.

64
Q

2 effects of improper stress response functioning

*estrogen and aging

A

bones = higher stress hormones can leach Ca2+ from bones, leading to osteoporosis.
hippocampal neurons are damaged by stress hormones. decrease dendritic trees and synapse. may regrow if stress is managed
*estrogen decreases with age. v low/none post-menopause. lose protective function in heart, bones.

65
Q

stress and aging/death - 2 animal studies

A

kinda like psychopathological death.

  1. salmon. stressful trip to native stream. have huge adrenal glands, peptic ulcers and decreased immune function (more parasites, infections).
    - - removal of adrenal gland after journey, fish live a year. adrenal gland in tact = live for 1 weak. hhigh glucocorticoid ffrom strss of journey leads to death
  2. marsupial mice. mating is strssful and competitive for males. have programmed death after single mating event. - high glucocorticoids be increased competition = death
66
Q

death after a single mating event

A

semelparity

67
Q

glucocorticoid regulation disrupted with age

A
  • cant initiate negative feedback responses of HPA axis. Higher baseline of glucocort when not stressed. = higher set point = more needed to initiate negative feedback response. if lower chronic stress but baseline stays high, set-point doesnt decrease.
68
Q

changes in set point btw stressed and non-stressed

-dexa

A

healthy/young: increase dexa = high glucocort = negative feedback actiavted to inhibit glucocort. DEXA RESPONSIVE
improper/old: add dexa high over set-point. no negative feedback. no decrease in natural glucocorticoids = DEXA RESISTANT

69
Q

hippocampus & negative feedback

A

glucocorticoids damage hippocampal neurons.
- high gluc receptors bc negative feedback. more glucocort receptors allow more sensitivity = normally signal to hypothalamus to stop releasing CRH.
with damage/age - fewer receptors - less likely to bind and initate the negative feedback response. causes set-point of negative feedback inhibition to increase = cycle.
can cause memory impairmets

70
Q

repeated sleep loss = jet lag and flight attendants &hippocampus

A

looked at flight attendants crossing time zones.
1 - given 5 days to recover btw flights
2 - given 15 days to recover from flights
* flight attendants for 5 years, controlled for time zones, looked at explicit mem and hippocampus size.
- less recovery: higher stress hormones, smaller hippocampus in 5 days vs 15 days.

71
Q

normal agin & hippocampus

A

increase baseline stress hormones = smaller hippocampus = increased baseline. cycle

72
Q

neurological insults + hippocampus

A

-in 2 ppl with same severity of stroke, th eone that has higher stress hormones at time of stroke will have more damage to hippcampus.

73
Q

PTSD + hippocampus.

A

ptsd = smaller hippocampus. but, which was is causal?
identical twin test: should have same hippocampal volume. - non trauma exposed: smaller hippocampas than average of his age. trauma exposed had even smaller hippocampus than twin. both were pre-disposed to ptsd (decreased ability to deal w stressor, regulte hormones), but an increase in a stressor, further promoted shrinking of hippocampus

74
Q

define ptsd

A

anxiety disorder associated with serious traumatic events. - symptoms include recurrent thoughts, images of trauma.

302 - final (6 decks)

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