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Physiological Psychology > Unit 3 Lecture > Flashcards

Unit 3 Lecture Flashcards

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1
Q

homeostasis

A
  • body maintains balance of EVERYTHING

- maintained by control mechanism

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2
Q

3 components of control mechanisms

A
  1. ) detector
  2. ) set-point
  3. ) effector
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3
Q

detector

A
  • where am i

- have to constantly check

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4
Q

set point

A

where you want to be

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5
Q

effector

A
  • how do I get there
  • activated when not where want to be
  • set point - detector = effector
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6
Q

cruise control

A
  • control mechanism
  • detector- spedometer
  • set-point: speed you set
  • effector- accelerator and brake (speed up or slow down)
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7
Q

too high blood sugar

A
  • viscosity of blood increases

- hard on heart

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8
Q

taking (erythropoietin) EPO

A
  • encourages bone marrow to make more RBCs
  • can deliver more O2 to tissues
  • side affect: blood sugar high
  • would have to take months before race (have to monitor always)
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9
Q

living at high altitude

A

-encourages bone marrow to make RBC

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10
Q

hypoglycemic shock

A
  • blood sugar too low

- bad for brain

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11
Q

detectors for glucostasis

A

-measure blood sugar in ventricle walls

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12
Q

set-point for glucostasis

A
  • set point in hypothalamus

- tells pancreas to release insulin

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13
Q

effector for glucostasis

A

-pancreas and liver

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14
Q

glucostasis

A
  • maintaining balance of blood sugar

- short therm

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15
Q

3 macro-nutrients

A
  1. ) fats
  2. ) sugars
  3. ) proteins
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16
Q

lipo-stasis

A
  • maintaining balance of fats

- long term

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17
Q

immediately after eating

A

pancreas releases insulin

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18
Q

insulin

A
  • hormone released from pancreas

- promotes conversion of sugar to fat

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19
Q

hormone

A

-chemical messenger

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20
Q

insulin effects

A
  • liver
  • adipose tissue
  • other tissues
  • causes different tissues to respond differently
  • makes blood sugar fall
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21
Q

insulin message to liver

A

-liver takes glucose and turns it into glycogen (starch)

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22
Q

insulin message to adipose tissue

A

-takes abundance of glucose and turns it into fat

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23
Q

insulin message to all other tissues

A

-turn glucose into energy required for activity

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24
Q

insulin and brain

A
  • insulin can’t get to brain
  • brain uses active transport to get glucose
  • only tissue no impacted by insulin release directly
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25
Q

3 ways to lower blood sugar

A
  1. ) turn to glycogen (liver)
  2. ) turn to fat (adipose)
  3. ) break for energy (other tissues)
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26
Q

glucagon

A
  • released when blood sugar drops
  • hormone
  • inhibits release of insulin
  • released ~4 hrs after eating
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27
Q

liver response to glucagon

A
  • turns glycogen back to glucose

* brain needs glucose

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28
Q

adipose response to glucagon

A
  • turn fat into fatty acids
  • can’t turn fat easily back into sugar
  • body can burn fatty acids instead of glucose when necessary
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29
Q

sugar

A
  • unconditioned stimulus that elicits unconditioned response of insulin release
  • results in blood sugar falling
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30
Q

classical conditioning and blood sugar

A
  • acquisition of association between neutral stimulus and unconditioned stimulus
  • Ex: package (ns) -> sugar (ucs) -> insulin
  • package becomes CS and insulin becomes CR
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31
Q

before meal

A
  • conditioned stimuli (smell, package, time, etc)
  • blood sugar spike
  • then blood sugar crash
  • it’s okay b/c you will present the actual sugar in the meal to go back to baseline
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32
Q

hungry before eat

A
  • not b/c short on energy

- because of learned conditioned stimulus

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33
Q

do diet drinks make you fat

A
  • rats given saccharin/sugar/plain water
  • something about sugar makes it ucs causing release of insulin (ucr)
  • sweet taste of artificial sweetener is cs, causing insulin release (cr) -> hungry
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34
Q

rats given water in diet drink experiment

A
  • control group
  • few drink calories
  • normal food calories
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35
Q

rats given glucose water in diet drink experiment

A
  • more drink calories
  • eat less food
  • total caloric intake same as control
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36
Q

rats given saccharin water

A
  • few drink calories

- food calories exceed control and glucose group

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37
Q

how can you not get fat from diet drinks

A

-drink after or with a meal b/c replenishing sugar at that time

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38
Q

advantage of human driver over cruise control

A
  • human driver speeds up before get to hill so that gears aren’t all stressed by cruise control
  • can use classical conditioning to predict future
  • same thing as noontime hunger
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39
Q

noontime hunger

A
  • preemptive reduction in glucose as a way to compensate for the inevitable increase in sugar
  • not intended to represent food shortage- why hunger fades away
  • just intended to prepare for oncoming sugar
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40
Q

insulin release cause dip in blood sugar

A

-converts glucose into glycogen, fat, or energy

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41
Q

Prader-Willy Syndrome

A
  • insulin levels always hight
  • not able to release sugar into the blood
  • turing it all into fat
  • would have continuously depleted blood sugar and you would continually turn it into fat
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42
Q

why are food ads conditioning experiment

A
  • see image of food
  • release insulin
  • blood sugar drops
  • call company of advertising for food (Ex: Dominos)
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43
Q

diet drinks ucs

A

sugar

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44
Q

diet drinks ucr

A

release insulin

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45
Q

diet drinks neutral stimulus

A

sweet tast

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46
Q

diet drinks cr

A

insulin release

*ucr and cr the same

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47
Q

diabetes mellitus

A
  • glucose in urine
  • extra glucose in blood excreted with water
  • “honey urine”
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48
Q

type 1 diabetes

A
  • auto-immune disorder
  • body thinks glucose is intruder
  • can’t make insulin
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49
Q

type 2 diabetes

A
  • relative insensitivity to insulin

- can make insulin, but cells are listening

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50
Q

satiety

A
  • feeling of being satisfied
  • feeling full
  • “quiet” signal compared to others
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51
Q

pleasure from eating

A

-resulting in obesity epidemic

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52
Q

taste

A
  • chemical analysis through tongue
  • sweet
  • sour
  • salty
  • bitter
  • umami
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53
Q

sweet

A
  • response to sugar- glucose, sucrose, fructose

- behavior response- want more

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54
Q

sour

A
  • respond to hydrogen ions (acids)

- behavior response- drool- dilutes acid

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55
Q

salty

A
  • response to Na+ ions

- behavior response- want more to certain point

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56
Q

bitter

A
  • response to OH-
  • behavioral response- spit it out
  • use higher cognition to develop taste for lettuce even though it is bitter (good for you)
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57
Q

umami

A
  • response to glutamate (AA)

- behavioral response- want more

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58
Q

taste of fat

A

-doesn’t have a flavor, but helps to spread other flavors around (fruit or bread)

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59
Q

spicy

A
  • response to capsaicin
  • behavioral response- heat/pain
  • good preservative- prevents bacterial growth
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60
Q

avian seed dispersal

A
  • birds don’t taste capsaicin as hot, but rather as sweet

- eat the peppers (etc) and spread across globe

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61
Q

why exercise is effective

A
  • since # calories burned during activity is small, speculation
  • don’t just burn calories during the actual exercise
    1. ) raise body temp for hours
    2. ) build muscle tissue
    3. ) serotonin release- hear satiety signal
    4. ) stress hormones released- endorphins (feel good) and glucagon (boosts blood sugar- not hungry after)
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62
Q

serotonin and subtle satiety signal

A

-appetite suppressant

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63
Q

SSRIs

A
  • antidepressant
  • serious side effects
  • can lead to weight gain
  • help with weight control b/c more serotonin quite other “voices” and increase effect of satiety “voice”
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64
Q

feelings of satiety

A
  1. ) stomach distension

2. ) duodenum distention

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65
Q

stomach distension

A
  • bulges
  • ghrelin (hormone) released into blood stream
  • tells you to stop eating
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66
Q

duodenum distention

A
  • releases cholecystokinin (CCK)
  • tells pyloric sphincter to close
  • food backs up into stomach
  • stimulates vagus nerve (implicated in digestion)
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67
Q

CCK

A
  • released in duodenum
  • signals brain to release
  • can’t use as weight loss product b/c CCK can’t cross BBB (brain has to make it directly)
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68
Q

mutant (obese) and normal mice

A
  • speculated the blood streams were different
  • made into siamese-twin mice
  • blood streams connected now
  • results: mutant mouse got skinny normal mouse stayed the same
  • normal mouse had leptin and Ob mouse didn’t
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69
Q

leptin

A
  • released when fat cells get big
    1. ) cranks up immune system
    2. ) suppresses appetite- negative feedback
    3. ) cranks up activity
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70
Q

why CCK not on market

A
  • pill broken in gut- need in brain

- injection still can’t cross BBB

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71
Q

why incentive to develop taste for spicy food

A

-food preservative

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72
Q

why obesity low in colorado

A
  • high altitude

- lots of elite athletes move there to increase RBC production

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73
Q

why is there an epidemic of obesity

A
  • high fructose corn syrup
  • brain has glucose and insulin detectors in ventricle walls
  • don’t have fructose detectors
  • deliver lots of calories in fructose form and not noticing that delivering b/c glucose receptors blind to fructose
  • Ex: drink coke and not any less hungry
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74
Q

Nixon’s farm subsidies

A
  • HFCS- 55% fructose, 42% glucose
  • lots of corn
  • extracted HFCS- where it originated
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75
Q

anorexia

A
  • “no appetite”- not really what it is
  • obsessed with food b/c starving
  • 0.5-2% of women
  • women 20x men
  • disorder of control- only way to control chaotic environment
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76
Q

anorexia and leptin levels

A
  • would expect them to have extra leptin based on the 3 leptin functions
  • not true, they have reduced leptin level- not a lack of the appetite
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77
Q

hypertrophism

A
  • male form of anorexia
  • increase in volume of organ or tissue
  • muscle are too big
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78
Q

electromyogram (EMG)

A
  • electrical activity in muscles

- measures muscle tone

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79
Q

electrooculogram (EOG)

A

-eye activity

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80
Q

electroencephalogram (EEG)

A

-measures brain activity

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81
Q

exogenous

A
  • externally generated

- cycle (cue): sun around earth

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82
Q

endogenous

A
  • internally generated

- cycle: inside your head

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83
Q

internal clock

A
  • 25 hours long
  • have to synchronize with exogenous cycle of sun
  • if no exogenous cycle, still would do stuff at similar times just a little off
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84
Q

m cells

A
  • in retina
  • detects motion
  • signaling is fast
  • magnocellular- big
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85
Q

p cells

A
  • in retina
  • detect shape and form
  • signaling is slow
  • parvocellular- small
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86
Q

k cells

A
  • in retina
  • detect- bright and dark
  • really slow
  • koniocellular- really small (powder)
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87
Q

is spring forward or fall back easier

A
  • spring forward lose an hour of sleep
  • spring- shortening day by hour
  • fall back- gain an hour of sleep
  • fall- lengthening day by hour
  • fall is easier b/c you’re technically on a 25 hour clock, so adding and hour is NATURAL
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88
Q

fall back and traffic

A

-fewer traffic accidents

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89
Q

optic chiasm

A

-site in brain where optic nerves cross

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90
Q

supra-chiasmatic nucleus

A
  • bundle of cells above optic chiasm

- where endogenous clock is

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91
Q

Gervil with ablated SCN

A
  • cut out SCN
  • gerbil acts like doesn’t have a clock
  • if transplant mutant (short cycle) or normal SCN cells, receiving will have that type of clock
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92
Q

why do we sleep

A
  1. ) repair/restoration
  2. ) helps us make a living (evolutionary)- save energy since hard to hunt at night
    * both true
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93
Q

Evidence for repair and restoration theory

A
  • after vigorous exercise sleep extra hours compared to normal
  • infants sleep a lot b/c constantly building cortex
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94
Q

unexplained repair and restoration theory

A
  • predators and prey
  • predators sleep a lot compared to prey
  • because prey is vulnerable to predation and often has to eat more b/c plants are food source
  • suggests that repair/restoration is not why we sleep
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95
Q

herbivore

A
  • sleep little (2 hrs/day)
  • subject to predation
  • low calorie food source, so have to constantly graze
96
Q

carnivore

A
  • sleep a lot (16 hrs/day)

- eat high calorie food, so don’t have to continually graze

97
Q

omnivores

A
  • sleep moderate hours (8 hrs/day)

- eat meat and plants

98
Q

dolphins

A
  • evidence that evolutionary and repair theory apply to sleep
  • figured out way to sleep for their lifestyle- they are air breathing swimmers
  • if they sleep they drown, therefore by evolutionary argument they don’t sleep (FALSE)
  • do sleep b/c need to repair
  • dolphin’s sleep patterns matches helping them earn a living
  • only one hemisphere of brain sleeps at a time
99
Q

evidence SCN generates circadian rhythm

A
  • Gerbils
  • recipient with ablated SCN gets donor cells and acts same way as donor did
  • If given normal -> act normal
  • if given mutant -> act mutant
100
Q

why is SCN above optic chiasm

A
  • need to be re-synchronized every day

- photoreceptors in retina allow for reset

101
Q

getting to sleep

A
  • have to decrease arousal
  • have to decrease temperature- slows processes
  • abundance of melatonin released from pineal gland
102
Q

why doesn’t melatonin help with insomnia

A
  • probably more an anxiety disorder, as opposed to a melatonin disorder
  • you’re already releasing melatonin when going to sleep, so taking more has no effect
103
Q

melatonin at times other than sleep

A
  • does knock you out

- Ex: eating turkey

104
Q

how many stages of sleep

A
  • 4

- deeper into sleep as progress through stages

105
Q

initial stage 1 sleep

A
  • think awake, but really asleep
  • easily confused with wakefulness
  • when you suddenly “jump”
106
Q

stages of sleep

A 
-wakeful
1- initial
2
3
2
1- emergent
*90 minute cycle
107
Q

light sleep

A
  • stage 1
  • EOG- eyes aren’t doing much
  • EEG- brain relatively energetic and organized
  • EMG- relatively high muscle tone
108
Q

deep sleep

A
  • stage 2 and 3
  • EOG- eyes aren’t doing much
  • EEG- little brain activity and chaotic
  • EMG- low muscle tone
109
Q

emergent stage 1

A
  • paradoxical b/c aspects are combo of characteristics of deep and light sleep
  • EEG- relatively energetic (light)
  • EMG- low muscle tone (deep)
110
Q

REM

A
  • rapid eye movement sleep
  • also has aspects of deep and light
  • relatively energetic
  • pons, limbic, parietal, and temporal activity
111
Q

when wake person up from REM

A
  • they say they are dreaming

- suggests that REM sleep is “dream” sleep

112
Q

REM rebound

A

-if deprived of REM, you try to make up for it and have multiple REM cycles

113
Q

high activity in pons during REM

A

-random signals to brain -> random dreams

114
Q

limbic system active during REM

A

-reason why scare self awake

115
Q

parietal cortex during REM

A
  • active during REM
  • spacial perception
  • later visual area that is active
116
Q

temporal cortex active during REM

A
  • facial perception

- later visual area that is active

117
Q

Inactivity during REM

A
  • V1- visual area
  • M1- paralysis during REM
  • frontal activity- degree depends on the individual
118
Q

abnormally high frontal cortical activity REM

A
  • implicated in lucid dreams
  • aware that you are dreaming
  • have ability to exert control over dream
  • as if conscious
119
Q

active parasympathetic

A
  • increase in digestion
  • increase immune system
  • enables penile erections
  • relaxed state
120
Q

social ridicule

A
  • causes fear rxn
  • Ex: laughed at when naked -> causes fear rxn to get naked in presence of others
  • sympathetic nervous system turns up (para turned down)
  • possible cause of ED
121
Q

causes of erectile dysfunction

A
  1. ) physical symptoms- nerve damage, BP problem

2. ) psychological- fear rxn

122
Q

why go to sleep lab for ED

A
  • every time anybody that CAN get erection goes into REM, they have an erection
  • even if not a sexual dream
  • during sleep, don’t have psychological symptoms
  • shows that ED is not a physical problem
  • women also get lubricated
123
Q

emergent stage 1

A
  • EOG
  • EMG- deep
  • EEG- light
  • paradoxical
  • similar to REM
124
Q

part of brain that is active during REM

A
  1. ) limbic system- accounts for emotional urgency
  2. ) pons- randomness
  3. ) temporal/parietal- face/place
  4. ) frontal cortex- lucid
125
Q

Insomnia

A
  • anxiety problem
  • can be onset- cant get to sleep
  • or can be termination- wake up often
126
Q

sleep apnea

A
  • wake up hundreds of times a night and not remember any of it (brief)
  • rarely experience emergent stage 1
  • wake up during stage 2
  • interrupted breathing and muscle tones
127
Q

narcolepsy

A
  • hypersomnia
  • fall asleep suddenly- straight into REM
  • cataplexy
128
Q

cataplexy

A
  • strong emotion

- sleep paralysis

129
Q

sleep paralysis

A
  • ease into wakefulness from REM

- only part of brain knows you’re awake

130
Q

therapy for sleep apnea

A
  • CPAP machine- addresses the loss of muscle tone- keeps airway open
  • lose weight
  • antihistamine- reduce inflammation
131
Q

narcolepsy therapy

A
  • stimulant

- actually need nice good sleep

132
Q

features of REM

A
  • low muscle tone

- paralysis- if occurs during wakening -> cataplexy

133
Q

psychoactive drugs

A
  • drugs that change the way we see and interpret the world

- exogenous

134
Q

administration of psychoactive drugs

A
  • has to pass BBB
  • has to be small or fat soluble
  • ingestion, inhalation, or injection
135
Q

slowest method of drug delivery

A
  • ingestion

- safest- can puke it out

136
Q

injection of drug fast response

A
  • if want to brain fast, inject into carotid artery

- hard to get to artery

137
Q

blood vessels on surface

A
  • veins

* arteries are deeper

138
Q

injection of drug into veins

A
  • has to go to heart, lungs, heart, then brain
  • not the fastest
  • injection most dangerous
139
Q

inhale a drug

A
  • lungs to heart to brain

- fastest way besides injecting into an artery

140
Q

snorting

A
  • not inhalation- not as fast
  • imbedding into mucus membranes
  • as fast as injection
  • safer than injection or inhalation
141
Q

metabolic tolerance of alcohol

A
  • liver adapts to produce more of the enzymes to break down alcohol in stomach
  • more liver NZ to break down means you have to drink more to get more of an effect
142
Q

cellular tolerance of cocaine

A
  • cocaine causes dopamine levels to be elevated
  • post-synaptic neurons constantly turned on
  • some receptor sites shut down
  • lose receptor sites for dopamine
  • can no longer experience pleasure unless have cocaine (need more)
143
Q

cross tolerance

A
  • tolerant for more than one drug that targets a specific neurotransmitter
  • Ex: cocaine is dopamine agonist -> crank up; meth also cranks you up, so crack addict would need more meth than novice drug user
144
Q

experienced user of cocaine

A
  • tolerate drugs that crank you up

- can’t tolerate heroin or morphine b/c they target endorphins, not dopamine

145
Q

behavioral tolerance

A
  • somebody who is drunk is not always a bad driver
  • if being drunk is a lifestyle behave better when drunk
  • can change behavior to suit different kinds of drugs
146
Q

how to get most out of illegal drugs

A

-pack with other white powder substances (ex: baby formula)

147
Q

conditioned drug use

A
  • present drug (UCS) to body, it releases NZ to break it down (UCR)
  • drug preps are neutral stimulus
  • present drugs after preps leads to NZ degradation
  • develop association for neutral stimulus- preps (CS) alone will cause enzymatic degradation (CR)
148
Q

Nth time taking drugs

A
  • preps are not longer neutral
  • preps are now conditioned stimulus
  • endorphines fall b/c of association with prep
  • will take more injection of drug to get to goal effect
  • presentation of cs (prep) and ucs (drug)
149
Q

conditioned withdrawal

A
  • need more drug to get intended effect b/c association of neutral stimulus (preps, setting, etc) causes endorphin levels to fall preparing for drug
  • have to have more drug to get to effect (recreational dose)
150
Q

presentation of ucs w/o cs

A
  • taking drug in different setting or new situation

- if take same amount as normal will overdose b/c didn’t preemptively withdraw (have endorphins fall) before injecting

151
Q

presentation of cs w/o ucs

A
  • present the preps, but don’t present the drugs
  • smell of nicotine, but no nicotine for quitters
  • have desperate need for cigarette when smell nicotine
152
Q

2 most addictive drugs

A
  1. ) nicotine

2. ) heroin

153
Q

2 ways of defining addiction

A
  1. ) is it the person that addicted

2. ) is it the drug that is addictive

154
Q

habitual users vs. addicts

A
  • addicts continues to take the drug in the face of social consequences
  • habitual users can stop if want to
155
Q

addicted person

A
  • continue to take drugs in the face of social consequences
  • physiology frontal cortex abnormalities- hard to control impulses and working memory
  • behavior- hard time imagining future
156
Q

difference between cocaine and heroin user

A
  • heroin is addictive, cocaine isn’t
  • behavioral and physiological differences
  • heroin user has frontal cortex degeneration
  • heroin users have a hard time imagining future
157
Q

Olds and Milner

A
  • studied physiological mechanism of addiction
  • rat in box with lever for food and lever for electrode
  • starving rat
158
Q

reward center in our brains

A
  • nucles accumbens
  • due to dopamine jolt
  • cocaine stimulates same part of brain
159
Q

pleasure

A
  • what motivates us
  • not necessarily immediate
  • cocaine is immediate pleasure
160
Q

mastery of experiences

A

-willing to endure cold to make it to the top of Mt. Everest

161
Q

what is an addictive drug

A
  • a drug that encourages basal ganglia to release dopamine

- stimulates nucleus accumbens (pleasure center)

162
Q

basal ganglia

A

-bundle of cells at bottom of brain

163
Q

substantia Nigra

A
  • part of basal ganglia

- dopaminergic- manufactures and releases dopamine

164
Q

nucleus accumbens

A
  • part of basal ganglia

- main target site of addictive drugs

165
Q

sources of pleasure

A
  1. ) sex
  2. ) eating
  3. ) socializing
  4. ) mastery of experiences
166
Q

habitual user dosage

A
  • have to take more compared to novice b/c
    1. ) build up tolerance
    2. ) have conditioned withdrawal
167
Q

4 reasons a habitual user can tolerate drug

A
  1. ) more NZ
  2. ) fewer receptor sites
  3. ) tolerate drugs that target same nt
  4. ) change behavior to be able to tolerate drug
168
Q

what happens if you present the cs but not the ucs

A

-feel yourself in desperate need for the drug (ucs)

169
Q

why is it cliche for someone to say “I can quit anytime I want”

A
  • if CAN, just a habitual user

- if CANT, considered an addict

170
Q

not addictive drugs

A
  • LSD

- Marijuana

171
Q

drug use

A
  • taking for clinical intended effects

- Ex: taking Ritalin and having better focus

172
Q

drug abuse

A
  • taking drug for fun

- Ex: taking Ritalin from friend

173
Q

mental disorders

A
  1. ) anxiety disorders
  2. ) mood disorders
  3. ) psychotic disorders
  4. ) personality disorders
174
Q

mood disorders

A
  1. ) major depression

2. ) bipolar disorder

175
Q

drugs for depression

A

-antidepressant

176
Q

bipolar disorder

A
  • have really great and really bad moods
  • drugs: mood stabilizer (lithium)
  • have to make highs not so high and lows not so low
177
Q

drugs for anxiety

A
  • anxiolytics- benzodiazepines
  • depressants
  • librium
  • xanax
  • valium
  • taken and abused recreationally
178
Q

drugs for psychotic disorders

A

-anti-psychotics

179
Q

drugs for personality disorders

A

-there are no drugs

180
Q

uppers

A

-stimulants

181
Q

downers

A

-depressants

182
Q

upper and downer

A

-narcotics

183
Q

hallucinogens

A
  • generates hallucinations
  • not an upper or downer
  • like a catch all b/c doesn’t fit in any of the other categories
  • Ex: marijuana
184
Q

drug categories

A
  1. ) uppers
  2. ) downers
  3. ) upper/downer
  4. ) hallucinogen
185
Q

cocaine

A
  • indirect dopamine agonist
  • traditional uses were coca chewing and tea
  • has medical uses
  • recreational uses
  • causes convulsions
  • upper drug (stimulant)
186
Q

Schedule 1 drug

A
  • potential for abuse

- no clinical uses

187
Q

Schedule 2 drug

A
  • potential for abuse
  • has clinical uses
  • Ex: cocaine
188
Q

cocaine clinical use

A
  • can be used as topical analgesic

- can also be used as topical vasoconstrictor

189
Q

cocaine recreational uses

A
  • cocaine hydrochloride

- snorted (mucus membrane) or inhaled (lungs)

190
Q

two most addictive substances

A
  1. ) heroin

2. ) nicotine

191
Q

drug self-administration in rats

A
  • heroin- press bar and stop later
  • nicotine- press bar and stop later
  • cocaine- don’t stop pressing bar until convulsions
192
Q

cocaine rat vs Olds/Milner rat

A
  • cocaine rat stopped pressing bar b/c of convulsions
  • Olds and Milner rat stopped pressing bar b/c of exhaustion
  • both stimulating pleasure center
193
Q

barbiturates

A
  • depressant (downer)
  • indirect GABA agonist
  • TI= 30 (have to take 30x effective dose to kill)
  • Ex: amo barbitol, quaalude
194
Q

therapeutic index

A

TI= LD50%/ ED50%

  • lethal dose for 50%/ effective dose for 50%
  • mg of drug/ kg of body weight
195
Q

TI for benzodiazepines

A
  • depressant (downer)
  • preferred of barbiturate
  • TI= 300
  • Ex: valium, xanax
196
Q

alcohol

A
  • depressant
  • yeast, antispetic, metablic enzymes
  • indirect GABA agonist (help GABA bind)
  • recreational uses
  • addictive
  • targets dopamine production and release
197
Q

GABA antagonist as sobriety drug

A
  • doesn’t work
  • makes you a wired drunk
  • they don’t work on the same parts of the brain
  • why you shouldn’t drink coffee with alcohol
  • Ex: alcohol suppresses cerebellum, while coffee stimulates basal ganglia
198
Q

parts of brain sensitive to alcohol

A
  1. ) cerebellum- why less coordinated
  2. ) frontal cortex- why impulsive
  3. ) amygdala- why less anxious
199
Q

caffeine

A
  • dopamine agonist

- stimulates basal ganglia

200
Q

why experimental GABA antagonist can’t be used

A
  • brain isn’t activated by the alcohol

- rest of body suffers from alcohol toxicity

201
Q

prevalence of depression

A
  • believed more prevalent among women
  • may not be true
  • women may just get treated more than men
  • men that are depressed may self-medicate
202
Q

type 1 alcoholism

A
  • equal prevalence in men and women

- most common type

203
Q

type 2 alcoholism

A
  • more prevalent in men
  • lower than normal drunkenness symptoms (cerebral and frontal suppression)
  • higher than normal anxiolytic effects- amygdala
204
Q

self-medicating in men

A
  • type 2 alcoholism
  • very successful at relieving anxiety
  • don’t get drunk
205
Q

narcotics

A
  • stimulant of nucleus accumbens (pleasure)
  • depressant of brainstem (life sustaining reflex)
  • direct endorphin agonist
  • morphine, heroin, analgesics, etc
206
Q

endorphin agonist

A
  • bind to and activate endorphin sites
  • morphine and heroin
  • analgesics
207
Q

heroin

A
  • when crosses BBB turns into morphine

- more fat soluble than morphine, so more efficient delivery to brain

208
Q

analgesic

A
  • pain reliever
  • aspirin acts at site of pain
  • morphine acts in brain
209
Q

brainstem

A
  • life sustaining reflexes
  • cough (why codeine fixes cough)
  • digestion
210
Q

endorphins and the utility of pain during stress

A
  • enorphins released under conditions of stress
  • why you can run w/ injury
  • internal pain reliever
211
Q

leprosy

A
  • not about flesh rotting off body
  • can’t feel pain, so don’t avoid dangers
  • hurt self without intending to
212
Q

narcan (naloxone)

A
  • counters effects of opiate overdose
  • opioid antagonist- binds to endorphin receptors and doesn’t activate
  • prevents narcotic from binding
  • prevents pain relief
  • targets FEELING aspect of pain
213
Q

placebo and acupuncture

A
  • cause you to release own endorphins

- essential like giving heroin

214
Q

narcan and acupuncture, heroin, morphine

A

-pain relief prevented

215
Q

narcan and hypnosis

A
  • doesn’t prevent pain releif

* suggests that hypnosis is not based on endorphin release- targets EMOTION aspect of pain

216
Q

aspects of pain

A
  1. ) feeling

2. ) emotion/motivation

217
Q

LSD and pain

A
  • not analgesic
  • does not reduce pain
  • if take with other analgesics makes pain less of priority for brain
218
Q

LSD and narcan

A
  • still have pain relief b/c LSD doesn’t target pain

- “placebo” pain

219
Q

what targets feeling aspect of pain

A
  • analgesics
  • narcan
  • acupuncture
220
Q

what targets emotional aspects of pain

A
  • LSD
  • hypnosis
  • placebo’s for pain
221
Q

Hallucinogens

A

-psychoactive drugs that cause changes in perception, emotion, consciousness, and thought

222
Q

LSD

A
  • not really a hallucinogen
  • doesn’t make you see something that isn’t there
  • stimulates what is already in your head
  • notice paths that things take
  • sensory stimulant
  • direct serotonin agonist
223
Q

iconic memory

A

-fast decaying store of visual information

224
Q

synestesia

A
  • senses together
  • see something, so hear something as result
  • hearing colors
225
Q

marijuana

A
  • not a hallucinogen or a narcotic
  • direct anandamide (blissful) agonist
  • hemp plant
  • schedule 1 drug
226
Q

resin

A
  • in bud of female hemp plant
  • source of marijuana
  • female plants aggressive, so makes more buds when male plant pollen taken away
  • reason why marijuana can be grown effectively and is so potent
227
Q

THC

A
  • agonist for cannabinoid receptor
  • suppresses release of nts in brain
  • active ingredient in marijuana
  • produces relaxed state and heightens senses
  • aka marinol
228
Q

Marinol

A
  • medical marijuana
  • primarily THC
  • anti-emitic- reduces nausea
  • increases appetite
  • common for cancer patients
229
Q

ingested Marinol vs smoked marijuana

A
  • essentially same substance
  • inhaled marijuana less effective anti-emitic
  • Marinol has more psychoactive metabolites than marijuana
230
Q

oncologist survey

A

-44% said they had recommended pot to patients

231
Q

1986 DEA hearings

A
  • Reagan asked if should make marijuana schedule 2 (medicinal)
  • panal said yes, but Reagan still overruled
232
Q

nucleus accumbens receptors

A

-no anandamide receptors

233
Q

brainstem receptors

A

-receptors for narcotics

234
Q

therapeutic index of marijuana

A
  • not lethal
  • not addictive
  • and has medicinal aspects
  • haven’t determined TI yet, but have established that rats can handle 5000x effective dose (doesn’t kill, just more stoned)
235
Q

drug (steroid) testing in athletes

A
  • not b/c enhances performance

- dangerous to yourself, so force others to engage in dangerous performance

Physiological Psychology (7 decks)

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