1
Q
homeostasis
A
- body maintains balance of EVERYTHING
- maintained by control mechanism
2
Q
3 components of control mechanisms
A
- ) detector
- ) set-point
- ) effector
3
Q
detector
A
- where am i
- have to constantly check
4
Q
set point
A
where you want to be
5
Q
effector
A
- how do I get there
- activated when not where want to be
- set point - detector = effector
6
Q
cruise control
A
- control mechanism
- detector- spedometer
- set-point: speed you set
- effector- accelerator and brake (speed up or slow down)
7
Q
too high blood sugar
A
- viscosity of blood increases
- hard on heart
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)
9
Q
living at high altitude
A
-encourages bone marrow to make RBC
10
Q
hypoglycemic shock
A
- blood sugar too low
- bad for brain
11
Q
detectors for glucostasis
A
-measure blood sugar in ventricle walls
12
Q
set-point for glucostasis
A
- set point in hypothalamus
- tells pancreas to release insulin
13
Q
effector for glucostasis
A
-pancreas and liver
14
Q
glucostasis
A
- maintaining balance of blood sugar
- short therm
15
Q
3 macro-nutrients
A
- ) fats
- ) sugars
- ) proteins
16
Q
lipo-stasis
A
- maintaining balance of fats
- long term
17
Q
immediately after eating
A
pancreas releases insulin
18
Q
insulin
A
- hormone released from pancreas
- promotes conversion of sugar to fat
19
Q
hormone
A
-chemical messenger
20
Q
insulin effects
A
- liver
- adipose tissue
- other tissues
- causes different tissues to respond differently
- makes blood sugar fall
21
Q
insulin message to liver
A
-liver takes glucose and turns it into glycogen (starch)
22
Q
insulin message to adipose tissue
A
-takes abundance of glucose and turns it into fat
23
Q
insulin message to all other tissues
A
-turn glucose into energy required for activity
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
25
3 ways to lower blood sugar
1. ) turn to glycogen (liver)
2. ) turn to fat (adipose)
3. ) break for energy (other tissues)
26
glucagon
- released when blood sugar drops
- hormone
- inhibits release of insulin
- released ~4 hrs after eating
27
liver response to glucagon
- turns glycogen back to glucose
| * brain needs glucose
28
adipose response to glucagon
- turn fat into fatty acids
- can't turn fat easily back into sugar
- body can burn fatty acids instead of glucose when necessary
29
sugar
- unconditioned stimulus that elicits unconditioned response of insulin release
- results in blood sugar falling
30
classical conditioning and blood sugar
- acquisition of association between neutral stimulus and unconditioned stimulus
- Ex: package (ns) -> sugar (ucs) -> insulin
- package becomes CS and insulin becomes CR
31
before meal
- 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
32
hungry before eat
- not b/c short on energy
| - because of learned conditioned stimulus
33
do diet drinks make you fat
- 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
34
rats given water in diet drink experiment
- control group
- few drink calories
- normal food calories
35
rats given glucose water in diet drink experiment
- more drink calories
- eat less food
- total caloric intake same as control
36
rats given saccharin water
- few drink calories
| - food calories exceed control and glucose group
37
how can you not get fat from diet drinks
-drink after or with a meal b/c replenishing sugar at that time
38
advantage of human driver over cruise control
- 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
39
noontime hunger
- 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
40
insulin release cause dip in blood sugar
-converts glucose into glycogen, fat, or energy
41
Prader-Willy Syndrome
- 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
42
why are food ads conditioning experiment
- see image of food
- release insulin
- blood sugar drops
- call company of advertising for food (Ex: Dominos)
43
diet drinks ucs
sugar
44
diet drinks ucr
release insulin
45
diet drinks neutral stimulus
sweet tast
46
diet drinks cr
insulin release
| *ucr and cr the same
47
diabetes mellitus
- glucose in urine
- extra glucose in blood excreted with water
- "honey urine"
48
type 1 diabetes
- auto-immune disorder
- body thinks glucose is intruder
- can't make insulin
49
type 2 diabetes
- relative insensitivity to insulin
| - can make insulin, but cells are listening
50
satiety
- feeling of being satisfied
- feeling full
- "quiet" signal compared to others
51
pleasure from eating
-resulting in obesity epidemic
52
taste
- chemical analysis through tongue
- sweet
- sour
- salty
- bitter
- umami
53
sweet
- response to sugar- glucose, sucrose, fructose
| - behavior response- want more
54
sour
- respond to hydrogen ions (acids)
| - behavior response- drool- dilutes acid
55
salty
- response to Na+ ions
| - behavior response- want more to certain point
56
bitter
- response to OH-
- behavioral response- spit it out
* use higher cognition to develop taste for lettuce even though it is bitter (good for you)
57
umami
- response to glutamate (AA)
| - behavioral response- want more
58
taste of fat
-doesn't have a flavor, but helps to spread other flavors around (fruit or bread)
59
spicy
- response to capsaicin
- behavioral response- heat/pain
* good preservative- prevents bacterial growth
60
avian seed dispersal
- birds don't taste capsaicin as hot, but rather as sweet
| - eat the peppers (etc) and spread across globe
61
why exercise is effective
- 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)
62
serotonin and subtle satiety signal
-appetite suppressant
63
SSRIs
- 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"
64
feelings of satiety
1. ) stomach distension
| 2. ) duodenum distention
65
stomach distension
- bulges
- ghrelin (hormone) released into blood stream
- tells you to stop eating
66
duodenum distention
- releases cholecystokinin (CCK)
- tells pyloric sphincter to close
- food backs up into stomach
- stimulates vagus nerve (implicated in digestion)
67
CCK
- 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)
68
mutant (obese) and normal mice
- 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
69
leptin
- released when fat cells get big
1. ) cranks up immune system
2. ) suppresses appetite- negative feedback
3. ) cranks up activity
70
why CCK not on market
- pill broken in gut- need in brain
| - injection still can't cross BBB
71
why incentive to develop taste for spicy food
-food preservative
72
why obesity low in colorado
- high altitude
| - lots of elite athletes move there to increase RBC production
73
why is there an epidemic of obesity
- 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
74
Nixon's farm subsidies
- HFCS- 55% fructose, 42% glucose
- lots of corn
- extracted HFCS- where it originated
75
anorexia
- "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
76
anorexia and leptin levels
- 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
77
hypertrophism
- male form of anorexia
- increase in volume of organ or tissue
- muscle are too big
78
electromyogram (EMG)
- electrical activity in muscles
| - measures muscle tone
79
electrooculogram (EOG)
-eye activity
80
electroencephalogram (EEG)
-measures brain activity
81
exogenous
- externally generated
| - cycle (cue): sun around earth
82
endogenous
- internally generated
| - cycle: inside your head
83
internal clock
- 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
84
m cells
- in retina
- detects motion
- signaling is fast
- magnocellular- big
85
p cells
- in retina
- detect shape and form
- signaling is slow
- parvocellular- small
86
k cells
- in retina
- detect- bright and dark
- really slow
- koniocellular- really small (powder)
87
is spring forward or fall back easier
- 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
88
fall back and traffic
-fewer traffic accidents
89
optic chiasm
-site in brain where optic nerves cross
90
supra-chiasmatic nucleus
- bundle of cells above optic chiasm
| - where endogenous clock is
91
Gervil with ablated SCN
- 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
92
why do we sleep
1. ) repair/restoration
2. ) helps us make a living (evolutionary)- save energy since hard to hunt at night
* both true
93
Evidence for repair and restoration theory
- after vigorous exercise sleep extra hours compared to normal
- infants sleep a lot b/c constantly building cortex
94
unexplained repair and restoration theory
- 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
95
herbivore
- sleep little (2 hrs/day)
- subject to predation
- low calorie food source, so have to constantly graze
96
carnivore
- sleep a lot (16 hrs/day)
| - eat high calorie food, so don't have to continually graze
97
omnivores
- sleep moderate hours (8 hrs/day)
| - eat meat and plants
98
dolphins
* 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
evidence SCN generates circadian rhythm
- 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
why is SCN above optic chiasm
- need to be re-synchronized every day
| - photoreceptors in retina allow for reset
101
getting to sleep
- have to decrease arousal
- have to decrease temperature- slows processes
- abundance of melatonin released from pineal gland
102
why doesn't melatonin help with insomnia
- 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
melatonin at times other than sleep
- does knock you out
| - Ex: eating turkey
104
how many stages of sleep
- 4
| - deeper into sleep as progress through stages
105
initial stage 1 sleep
- think awake, but really asleep
- easily confused with wakefulness
- when you suddenly "jump"
106
stages of sleep
```
-wakeful
1- initial
2
3
2
1- emergent
*90 minute cycle
```
107
light sleep
- stage 1
- EOG- eyes aren't doing much
- EEG- brain relatively energetic and organized
- EMG- relatively high muscle tone
108
deep sleep
- stage 2 and 3
- EOG- eyes aren't doing much
- EEG- little brain activity and chaotic
- EMG- low muscle tone
109
emergent stage 1
- paradoxical b/c aspects are combo of characteristics of deep and light sleep
- EEG- relatively energetic (light)
- EMG- low muscle tone (deep)
110
REM
- rapid eye movement sleep
- also has aspects of deep and light
- relatively energetic
- pons, limbic, parietal, and temporal activity
111
when wake person up from REM
- they say they are dreaming
| - suggests that REM sleep is "dream" sleep
112
REM rebound
-if deprived of REM, you try to make up for it and have multiple REM cycles
113
high activity in pons during REM
-random signals to brain -> random dreams
114
limbic system active during REM
-reason why scare self awake
115
parietal cortex during REM
- active during REM
- spacial perception
- later visual area that is active
116
temporal cortex active during REM
- facial perception
| - later visual area that is active
117
Inactivity during REM
- V1- visual area
- M1- paralysis during REM
- frontal activity- degree depends on the individual
118
abnormally high frontal cortical activity REM
- implicated in lucid dreams
- aware that you are dreaming
- have ability to exert control over dream
- as if conscious
119
active parasympathetic
- increase in digestion
- increase immune system
- enables penile erections
* relaxed state
120
social ridicule
- 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
causes of erectile dysfunction
1. ) physical symptoms- nerve damage, BP problem
| 2. ) psychological- fear rxn
122
why go to sleep lab for ED
- 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
emergent stage 1
- EOG
- EMG- deep
- EEG- light
* paradoxical
* similar to REM
124
part of brain that is active during REM
1. ) limbic system- accounts for emotional urgency
2. ) pons- randomness
3. ) temporal/parietal- face/place
4. ) frontal cortex- lucid
125
Insomnia
- anxiety problem
- can be onset- cant get to sleep
- or can be termination- wake up often
126
sleep apnea
- 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
narcolepsy
- hypersomnia
- fall asleep suddenly- straight into REM
- cataplexy
128
cataplexy
- strong emotion
| - sleep paralysis
129
sleep paralysis
- ease into wakefulness from REM
| - only part of brain knows you're awake
130
therapy for sleep apnea
- CPAP machine- addresses the loss of muscle tone- keeps airway open
- lose weight
- antihistamine- reduce inflammation
131
narcolepsy therapy
- stimulant
| - actually need nice good sleep
132
features of REM
- low muscle tone
| - paralysis- if occurs during wakening -> cataplexy
133
psychoactive drugs
- drugs that change the way we see and interpret the world
| - exogenous
134
administration of psychoactive drugs
- has to pass BBB
- has to be small or fat soluble
- ingestion, inhalation, or injection
135
slowest method of drug delivery
- ingestion
| - safest- can puke it out
136
injection of drug fast response
- if want to brain fast, inject into carotid artery
| - hard to get to artery
137
blood vessels on surface
- veins
| * arteries are deeper
138
injection of drug into veins
- has to go to heart, lungs, heart, then brain
- not the fastest
* injection most dangerous
139
inhale a drug
- lungs to heart to brain
| - fastest way besides injecting into an artery
140
snorting
- not inhalation- not as fast
- imbedding into mucus membranes
- as fast as injection
- safer than injection or inhalation
141
metabolic tolerance of alcohol
- 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
cellular tolerance of cocaine
- 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
cross tolerance
- 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
experienced user of cocaine
- tolerate drugs that crank you up
| - can't tolerate heroin or morphine b/c they target endorphins, not dopamine
145
behavioral tolerance
- 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
how to get most out of illegal drugs
-pack with other white powder substances (ex: baby formula)
147
conditioned drug use
- 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
Nth time taking drugs
- 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
conditioned withdrawal
- 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
presentation of ucs w/o cs
- 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
presentation of cs w/o ucs
- 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
2 most addictive drugs
1. ) nicotine
| 2. ) heroin
153
2 ways of defining addiction
1. ) is it the person that addicted
| 2. ) is it the drug that is addictive
154
habitual users vs. addicts
- addicts continues to take the drug in the face of social consequences
- habitual users can stop if want to
155
addicted person
- 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
difference between cocaine and heroin user
- 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
Olds and Milner
- studied physiological mechanism of addiction
- rat in box with lever for food and lever for electrode
- starving rat
158
reward center in our brains
- nucles accumbens
- due to dopamine jolt
- cocaine stimulates same part of brain
159
pleasure
- what motivates us
- not necessarily immediate
- cocaine is immediate pleasure
160
mastery of experiences
-willing to endure cold to make it to the top of Mt. Everest
161
what is an addictive drug
- a drug that encourages basal ganglia to release dopamine
| - stimulates nucleus accumbens (pleasure center)
162
basal ganglia
-bundle of cells at bottom of brain
163
substantia Nigra
- part of basal ganglia
| - dopaminergic- manufactures and releases dopamine
164
nucleus accumbens
- part of basal ganglia
| - main target site of addictive drugs
165
sources of pleasure
1. ) sex
2. ) eating
3. ) socializing
4. ) mastery of experiences
166
habitual user dosage
- have to take more compared to novice b/c
1. ) build up tolerance
2. ) have conditioned withdrawal
167
4 reasons a habitual user can tolerate drug
1. ) more NZ
2. ) fewer receptor sites
3. ) tolerate drugs that target same nt
4. ) change behavior to be able to tolerate drug
168
what happens if you present the cs but not the ucs
-feel yourself in desperate need for the drug (ucs)
169
why is it cliche for someone to say "I can quit anytime I want"
- if CAN, just a habitual user
| - if CANT, considered an addict
170
not addictive drugs
- LSD
| - Marijuana
171
drug use
- taking for clinical intended effects
| - Ex: taking Ritalin and having better focus
172
drug abuse
- taking drug for fun
| - Ex: taking Ritalin from friend
173
mental disorders
1. ) anxiety disorders
2. ) mood disorders
3. ) psychotic disorders
4. ) personality disorders
174
mood disorders
1. ) major depression
| 2. ) bipolar disorder
175
drugs for depression
-antidepressant
176
bipolar disorder
- have really great and really bad moods
- drugs: mood stabilizer (lithium)
- have to make highs not so high and lows not so low
177
drugs for anxiety
- anxiolytics- benzodiazepines
- depressants
- librium
- xanax
- valium
* taken and abused recreationally
178
drugs for psychotic disorders
-anti-psychotics
179
drugs for personality disorders
-there are no drugs
180
uppers
-stimulants
181
downers
-depressants
182
upper and downer
-narcotics
183
hallucinogens
- 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
drug categories
1. ) uppers
2. ) downers
3. ) upper/downer
4. ) hallucinogen
185
cocaine
- indirect dopamine agonist
- traditional uses were coca chewing and tea
- has medical uses
- recreational uses
- causes convulsions
- upper drug (stimulant)
186
Schedule 1 drug
- potential for abuse
| - no clinical uses
187
Schedule 2 drug
- potential for abuse
- has clinical uses
- Ex: cocaine
188
cocaine clinical use
- can be used as topical analgesic
| - can also be used as topical vasoconstrictor
189
cocaine recreational uses
- cocaine hydrochloride
| - snorted (mucus membrane) or inhaled (lungs)
190
two most addictive substances
1. ) heroin
| 2. ) nicotine
191
drug self-administration in rats
- heroin- press bar and stop later
- nicotine- press bar and stop later
- cocaine- don't stop pressing bar until convulsions
192
cocaine rat vs Olds/Milner rat
- 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
barbiturates
- depressant (downer)
- indirect GABA agonist
- TI= 30 (have to take 30x effective dose to kill)
- Ex: amo barbitol, quaalude
194
therapeutic index
TI= LD50%/ ED50%
- lethal dose for 50%/ effective dose for 50%
- mg of drug/ kg of body weight
195
TI for benzodiazepines
- depressant (downer)
- preferred of barbiturate
- TI= 300
- Ex: valium, xanax
196
alcohol
- depressant
- yeast, antispetic, metablic enzymes
- indirect GABA agonist (help GABA bind)
- recreational uses
- addictive
- targets dopamine production and release
197
GABA antagonist as sobriety drug
- 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
parts of brain sensitive to alcohol
1. ) cerebellum- why less coordinated
2. ) frontal cortex- why impulsive
3. ) amygdala- why less anxious
199
caffeine
- dopamine agonist
| - stimulates basal ganglia
200
why experimental GABA antagonist can't be used
- brain isn't activated by the alcohol
| - rest of body suffers from alcohol toxicity
201
prevalence of depression
- 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
type 1 alcoholism
- equal prevalence in men and women
| - most common type
203
type 2 alcoholism
- more prevalent in men
- lower than normal drunkenness symptoms (cerebral and frontal suppression)
- higher than normal anxiolytic effects- amygdala
204
self-medicating in men
- type 2 alcoholism
- very successful at relieving anxiety
- don't get drunk
205
narcotics
- stimulant of nucleus accumbens (pleasure)
- depressant of brainstem (life sustaining reflex)
- direct endorphin agonist
- morphine, heroin, analgesics, etc
206
endorphin agonist
- bind to and activate endorphin sites
- morphine and heroin
- analgesics
207
heroin
- when crosses BBB turns into morphine
| - more fat soluble than morphine, so more efficient delivery to brain
208
analgesic
- pain reliever
- aspirin acts at site of pain
- morphine acts in brain
209
brainstem
- life sustaining reflexes
- cough (why codeine fixes cough)
- digestion
210
endorphins and the utility of pain during stress
- enorphins released under conditions of stress
- why you can run w/ injury
- internal pain reliever
211
leprosy
- not about flesh rotting off body
- can't feel pain, so don't avoid dangers
- hurt self without intending to
212
narcan (naloxone)
- 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
placebo and acupuncture
- cause you to release own endorphins
| - essential like giving heroin
214
narcan and acupuncture, heroin, morphine
-pain relief prevented
215
narcan and hypnosis
- doesn't prevent pain releif
| * suggests that hypnosis is not based on endorphin release- targets EMOTION aspect of pain
216
aspects of pain
1. ) feeling
| 2. ) emotion/motivation
217
LSD and pain
- not analgesic
- does not reduce pain
- if take with other analgesics makes pain less of priority for brain
218
LSD and narcan
- still have pain relief b/c LSD doesn't target pain
| - "placebo" pain
219
what targets feeling aspect of pain
- analgesics
- narcan
- acupuncture
220
what targets emotional aspects of pain
- LSD
- hypnosis
* placebo's for pain
221
Hallucinogens
-psychoactive drugs that cause changes in perception, emotion, consciousness, and thought
222
LSD
- 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
iconic memory
-fast decaying store of visual information
224
synestesia
- senses together
- see something, so hear something as result
- hearing colors
225
marijuana
- not a hallucinogen or a narcotic
- direct anandamide (blissful) agonist
- hemp plant
- schedule 1 drug
226
resin
- 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
THC
- agonist for cannabinoid receptor
- suppresses release of nts in brain
- active ingredient in marijuana
- produces relaxed state and heightens senses
* aka marinol
228
Marinol
- medical marijuana
- primarily THC
- anti-emitic- reduces nausea
- increases appetite
- common for cancer patients
229
ingested Marinol vs smoked marijuana
- essentially same substance
- inhaled marijuana less effective anti-emitic
- Marinol has more psychoactive metabolites than marijuana
230
oncologist survey
-44% said they had recommended pot to patients
231
1986 DEA hearings
- Reagan asked if should make marijuana schedule 2 (medicinal)
- panal said yes, but Reagan still overruled
232
nucleus accumbens receptors
-no anandamide receptors
233
brainstem receptors
-receptors for narcotics
234
therapeutic index of marijuana
- 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
drug (steroid) testing in athletes
- not b/c enhances performance
| - dangerous to yourself, so force others to engage in dangerous performance
Physiological Psychology
flashcards
Decks in class (7)
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