BioPsych Exam 2 Flashcards

1
Q

Suprachiasmatic Nucleus

A

“Biological clock”
located in hypothalamus

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2
Q

Chronotype

A

shift of circadian rhythm
young- night owls
old- early bird

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3
Q

Process-S

A

sleep drive
impacted by level of activity and outside factors
mental labor causes a stronger sleep drive than physical labor

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4
Q

Process-C

A

wake drive

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5
Q

Restorative Theory

A

repair and regenerate body
muscle repair, tissue growth, increased protein synthesis, growth hormone release
neuroplasticity increases while sleeping

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6
Q

Elimination Theory

A

gets rid of excess sensory info
synaptic pruning and strengthening

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7
Q

Brain Plasticity Theory

A

Neural reorganization, growth of neurons and brain structures

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8
Q

Immobilization Theory

A

Sleep is innate response with species-specific patterns
keeps on inactive and safe during least efficient part of day/night cycle

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9
Q

Energy Conservation Theory

A

following survival activities
energy expenditure decreases when sleeping
10% decrease in metabolic rate

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10
Q

fatal familial insomnia

A

prions destroy neurons in thalamus
genetic mutation: first lose ability to have SWS, then REM, then unable to fall asleep, die within 6 months

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11
Q

Lack of SWS correlates with…

A

greater risk for cardiovascular disease, diabetes, obesity

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12
Q

Functions of REM sleep

A

promote brain growth
facilitate learning
consolidation of nondeclarative memory
REM rebound phenomenon
- if you pull an all-nighter you will make up REM sleep first, then SWS rebound
less REM sleep under influence

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13
Q

Electroencephalogram

A

(EEG)
electrical potential recorded from electrodes placed on scalp (“brain waves”)
detects neural activity/firing

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14
Q

Electrooculogram

A

EOG
measure of eye movements seen during sleep, detects muscle firing
SWS: slow rolling eye movements
REM: fast, left to right

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15
Q

Electromyogram

A

EMG
electrical potential recorded from an electrode placed on muscle (ex. arm or thigh)
measures changed in muscle tension/activity particularly in face and neck muscles
NO MUSCLE TONE DURING REM SLEEP
Mentalis muscle loses all tone as soon as you fall asleep, distinguishes sleep vs. wakefulness

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16
Q

Passive Theory of Sleep

A

proposed sleep is passive because it cuts off sensory input during surgery

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17
Q

-Cerveau isole

A

-separated forebrain from hindbrain
-cats did not wake up on their own

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18
Q

Encephale isole

A
  • separated brain from spinal cord
  • cats had normal sleep/wake cycles
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19
Q

Active Theory of sleep

A
  • discovered Reticular Formation
  • proposed sleep is inactive and the brain actively regulates sleep-wake cycle
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20
Q

stage 1 sleep

A

transition from wake-sleep (1-7 minutes)

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21
Q

stage 2 sleep

A

about 70-75% of nights sleep
- can last 10-25 minutes
- REM gets longer as night goes on
- spend more time dreaming towards morning

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22
Q

stage 3 sleep

A
  • SWS
  • long waves on EEG
  • about 20-40 minutes
  • harder to wake up from
  • gets shorter towards morning
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23
Q

Gamma waves

A
  • small and close together
  • irregular, low amp
  • highest frequency is about 30-120 Hz
  • occurs at hyperfocus, concentration
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24
Q

Beta waves

A
  • medium size
  • irregular, low amp, highest frequency about 13-30 Hz
  • occur during the day
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25
Q

Alpha waves

A
  • big and far apart
  • fairly regular, low amp, high frequency about 8-13 Hz
  • occur during relaxation
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26
Q

Theta waves

A
  • low amp, moderate frequency about 4-8 Hz
  • occur during stage 2 sleep
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27
Q

Sleep Spindles

A
  • short burst of about 12-14 Hz
  • in between theta waves
  • slow progression as we age (kids sleep better)
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28
Q

K complexes

A

sudden sharp waveforms

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29
Q

Delta waves

A
  • fairly regular, high amp, low frequency about 1-4 Hz
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30
Q

REM sleep (paradoxical sleep)

A

a wave of beta and a wave of alpha
- (sleep and wake waves)

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31
Q

Acetylcholine (cholinergic neuron)

A
  • dorsal pons and basal forebrain
  • plays role in arousal of cerebral cortex
  • levels high during wakefulness and REM sleep
  • project to and impact medial pons, thalamus and cortex
  • involved in cortex and hippocampus arousal
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32
Q

Norepinephrine (noradrenergic neuron)

A
  • plays role in attention and vigilance
  • levels high only during wakefulness
  • project to impact thalamus, hippocampus, cerebellum, pons and medulla
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33
Q

Serotonin (serotonergic neuron) (5-HT)

A
  • levels high during wakefulness
  • levels fall as descending towards REM sleep
  • cortical and behavioral arousal
  • plays role in activating behavior (pacing, chewing, grooming in rodents)
  • project to impact thalamus, hypothalamus, cortex, hippocampus, basal ganglion
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34
Q

Histamine

A
  • levels high during wakefulness
  • levels low during SWS and REM sleep
  • implicated in control of wakefulness and arousal
  • project to and impact cortex, thalamus, hypothalamus, basal ganglia, basal forebrain
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35
Q

Orexin

A
  • from lateral hypothalamus
  • levels high during wakefulness
  • levels low during rest and all sleep stages
  • increase activity in the brainstem and forebrain arousal systems
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36
Q

vIPOA

A

Ventrolateral preoptic area

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37
Q

vIPAG

A

ventrolateral periaqueductal area

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38
Q

SLD

A

sublaterodorsal nucleus

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39
Q

GABA

A
  • from vIPOA
  • suppress alertness and behavioral arousal
  • promote sleep
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40
Q

Adenosine

A

Peptide released by neurons during high levels of metabolic activity throughout the day
- increases activity on the vIPOA

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41
Q

Cataplexy

A

muscle weakness while a person is awake
- can be caused by high emotion

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42
Q

sleep paralysis

A

loss of muscle tone as we fall asleep or wake up
- SLD activation before falling asleep
- SLD deactivation after waking up

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43
Q

2 types of Hallucinations

A
  • hypnagogic
  • hypnopompic
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44
Q

Hypnagogic

A
  • SLD nucleus is starting to activate
  • people will see “ghosts” or people who arent there
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45
Q

Hypnopompic

A

-delay between REM turning off
- SLD is still firing, causes dream to continue as people open their eyes

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46
Q

Narcolepsy

A
  • difficulty staying awake during the day
  • difficulty staying asleep during the night
  • “skip” SWS and enter REM quickly
47
Q

causes of narcolepsy

A
  • deficiency of peptide neurotransmitter orexin
  • in canines, Orexin B receptor
  • in humans, complete absence of Orexin
48
Q

Treatment of Narcolepsy

A

Ritalin: dopamine and norepinephrine agonist (Reuptake inhibitor)
Amphetamine: dopamine and norepinephrine agonist (reuptake inhibitor)
Modafinil (Provigil): orexin agonist (reduces daytime sleepiness

49
Q

SSRIs and SNRIs

A

Fluoxetine
Venlafaxine
Atomoxetine
- reduce episodes of REM sleep components

50
Q

Tricyclic antidepressants

A

norepinephrine, serotonin, dopamine agonist
Protriptyline (vivactil)
Imipramine (tofranil)
- reduce episodes of REM sleep components

51
Q

Sodium Oxybate (Xyrem)

A
  • CNS depressant that reduces excessive daytime sleepiness and cataplexy
  • GABA-B receptor agonist (increases GABA)
  • reduces daytime sleepiness, stay asleep through the night
52
Q

Swyer Syndrome

A

46 XY genotype
15-20% SRY gene
- Appears as female but is missing the SRY gene on Y chromie
- non-functioning ovaries
- doesn’t start period
- take supplemental estrogen

53
Q

46 XX Testicular Disorder

A

SRY gene is misplaces onto X chromosome
- development of male genitalia
- smaller testes and infertility may occur

54
Q

Differentiation occurs at…

A

2nd and 3rd prenatal months

55
Q

wolffian system

A

(male duct)
- prostate
- seminal vesicle
- male duct
- gonad

56
Q

Mullerian System

A

(female duct)
- vagina
- Uterus
- Female duct (fallopian tube)
- Gonad

57
Q

As testis develop…

A
  • Mullerian-inhibiting substance (MIS) and testosterone are synthesized and released
  • 5-alpha converts testosterone into dihydrotestosterone
58
Q

must have dihydrotestosterone to…

A

develop a penis and scrotum

59
Q

5-alpha-reductase deficiency syndrome

A

lack of 5-alpha- reductase
- born looking female, grow up looking male

60
Q

female brains have…

A
  • higher percentage of gray matter
  • larger hippocampus
  • larger ventral prefrontal cortex
  • high levels of serotonin, dopamine, GABA
61
Q

Male brains have…

A
  • 10% larger cerebral hemispheres
  • higher percentage of white matter and cerebral spinal fluid
  • larger and more reactive amygdala
  • larger hypothalamus
62
Q

aromatase

A

converts testosterone into estradiol

63
Q

alpha fetoprotein

A
  • produced by fetal liver cells and placenta during fetal development
  • binds circulating estradiol and prevents its entry into brain
  • does not bind to testosterone
64
Q

Hypothalamic-pituitary-gonadal axis

A

Paraventricular nucleus and supraoptic nucleus directly release hormones through posterior pituitary portal
- such as oxytocin

65
Q

Anterior pituitary

A

releases gonadotropins
- Follicle-stimulating hormone
- luteinizing hormone

66
Q

FSH

A
  • ova development
  • sperm development
  • increase estradiol production
67
Q

LH

A
  • stimulates testosterone secretion
  • from Leydig cells in testes
  • from Theca cells in ovaries
  • LH surge triggers ovulation
68
Q

Gonadal hormones

A
  • androgens
  • estrogens
  • gestagens
69
Q

Androgens

A

ex. Testosterone
- Leydig cells in testes
- Theca cells in ovaries

70
Q

androgens are responsible for…

A
  • growth and repair of reproductive cells
  • Development of bone mass
  • Development of hair in puberty in females
  • Development of hair in males (facial, body)
  • Maturation of sperm
  • Secondary sex characteristics in males during puberty
71
Q

Estrogens

A

ex. estradiol
- converted from testosterone by aromatase

72
Q

estrogens are responsible for…

A
  • Thickening uterine wall
  • Maturation of eggs
  • Sex drive
  • Erections in males
73
Q

Gestagens

A

ex. progesterone
- important role in female fertility and reproduction

74
Q

Gestagens are responsible for…

A

Thinking of uterine lining
“Pregnancy hormone”
High during pregnancy
Low levels can cause a miscarriage
Prohibits contraction of uterus during labor
Maybe involved in the creation of sperm?

75
Q

combination pill

A

delivers both estrogen and progestin for 3 weeks

76
Q

how does the combination pill work?

A

Estrogen decreases secretion of FSH
- Estrogen starts on day 1 of cycle, given for about 3 weeks, then interferes with FSH
FSH is being reduced, no additional estradiol from ovaries, comes from the pill instead
- Reduction of pulsing from hypothalamus
Progestin prevents secretion of LH

77
Q

Plan B

A
  • stops the release of ovum
  • Prevents ovulation from occurring when sperm is still viable
    24 hours, 95% effective
    24-72 hours, 89% effective
78
Q

Mifepristone

A
  • progesterone receptor blocker
  • stop pregnancy from continuing
    — uterine wall deteriorates
    — placenta detaches
  • used to end early pregnancy (within 70 days or less since last menstrual period
  • followed by Misopristol
    — causes uterine contractions
    — softens and dilates cervix
79
Q

Medial Preoptic Area (MPA of hypothalamus) (males)

A
  • Involved in regulation of male sexual behavior in rodents
  • Drives behaviors, impacted by testosterone
    — erections
    — Mounting of female
    — Thrusting/ejaculation
  • Damaged can cause behaviors to not occur
80
Q

Lee-Boot effect

A
  • Groups and colonies that are matriarchal
  • without presence of males , cycles sync and stop
  • If male becomes present within 48 hours, go into estrice
81
Q

Whitten effect

A
  • Group of females housed together, estrice cycles sync and go into estrice at same time, synced cycles
82
Q

Bruce effect

A
  • Colony of females with one dominant male
  • When a new male takes over, any females that are starting pregnancy with prior male, the eggs will not plant
  • Pheromones from new male can cause miscarriage
83
Q

Vandenbergh effect

A
  • Matriarchal clones, introduction of male accelerates sexual maturity in young female (accelerates puberty)
84
Q

Ventromedial nucleus (VMN of hypothalamus) (females)

A
  • regulation of female sexual behavior in rodents
  • stimulate arousal
85
Q

Lordosis posture

A

(throwing it back)
- driven by higher levels of estradiol being released during estrice
- more estradiol, more activation of VMN

86
Q

ingestion

A
  • pills
  • easy to administer
  • relatively safe
  • takes time for medication to break down, allows time for intervention in case of side effect
87
Q

downsides of ingestion

A
  • unpredictability of dosing (“must be taken with food”)
  • some drugs can be deactivated as soon as they hit the stomach
88
Q

subcutaneous injection

A
  • injection in fatty layer between skin and muscle
    ex. insulin
89
Q

intramuscularly (IM) injection

A

injected in large muscles
ex. vaccines

90
Q

intravenous (IV) injection

A

injected directly into bloodstream
- strongest, fastest, and most predictable

91
Q

downsides of intravenous injection

A
  • risk of overdose
  • use of same needle can lead to infection
  • only so many places to inject
    — people who abuse injection develop scar tissue or collapsed veins
92
Q

Inhalation

A
  • directed into bloodstream through the lungs
    ex. nicotine, THC, asthma meds
  • lower dosage than ingestion and injection
93
Q

downsides of inhalation

A
  • depends how strongly they inhale
  • has to be a particular dose
  • lung damage
94
Q

Absorption

A
  • through lining of nose or mouth
    ex. chewing tobacco, nicotine pouches, snorting cocaine
  • quicker than ingestion
95
Q

downsides of absorption

A
  • relies on tissue you place substance in
  • repeated use, tissue becomes scarred and not as effective
  • causes deterioration or ulceration
96
Q

tolerance

A

less reactivity to substance

97
Q

Functional tolerance

A
  • response to drug is decreased by cellular mechanisms
    ex. receptor changes
98
Q

Metabolic tolerance

A
  • decrease in amount of drug that reaches the target site
  • the more repetition of drug use, the body changes to get rid or deactivate it faster
99
Q

conditioned tolerance

A

environmental cues activate a compensatory response that counteract the drug effect
ex. alcohol causes a decrease in body temp, can cause hypothermia

100
Q

Intracranial Self-Stimulation (ICSS)

A

rat presses lever themself
- implanted electrode on hypothalamus, continue to press the lever for stimulation

101
Q

Conditioned place preference

A
  • rats hang out in chamber if they liked the drug
  • avoids chamber if they didn’t like it
102
Q

Positive Reinforcement

A
  • drug-taking behavior is followed by a pleasant outcome of the drug
  • seek out drug again
103
Q

Negative reinforcement

A
  • drug-taking behavior is followed by the removal of an unpleasant event
  • feel relief; seek out drug again
104
Q

Physical dependence theory of addiction

A

physical changes start to show, so they take the drug for withdrawal symptoms to go away
- negative reinforcement

105
Q

Positive Incentive Theory of addiction

A

the drug makes you feel good so that’s why you take it
- positive reinforcement

106
Q

Incentive Sensitization theory of addiction

A

after tolerance develops, changes the craving for the drug, remembers how it used to make them feel good so they keep taking it
- positive reinforcement

107
Q

What are the 3 pathways in the Mesotelencephalic Dopamine System

A
  • nigrostriatal pathway
  • mesolimbic pathway
  • mesocortical pathway
108
Q

Nigrostriatal pathway

A
  • starts in substantianigra, ends in dorsal striatum
    — deteriorates early in parkinson’s disease
109
Q

Mesolimbic pathway

A
  • ventral tegmental area
    — stimulating dopamine release has an effect on emotional experience
    — (rewarding effects)
110
Q

Mesocortical pathway

A
  • ventral tegmental area to prefrontal cortex
    — remembering how the drug made you feel (incentive sensitization theory)
111
Q

mapping studies

A

indicate that areas that support ICSS are typcally part of the mesotelencephalic dopamine system

112
Q

Lesion studies

A

show that 6-hydroxydopamine chemical lesions disrupts ICSS
— (destroys dopamine)

113
Q

Antagonist studies

A

show that dopamine antagonists decrease ICSS
— once you stop dopamine receptors, rats stop pressing lever

114
Q

Agonist studies

A

show that dopamine agonists increase ICSS