Unit 3 Multiple Choice and Short Answer Flashcards

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1
Q

general consequences of lack of sleep

A
  1. Lower motivation
  2. Impaired judgement
  3. Slower cognitive processing
  4. More errors/accidents, even risk of death
  5. Weight gain (cravings)
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2
Q

What is the longest a human has gone without sleep?

A

11 days (264 hours)

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3
Q

lack of sleep as a fatality

A
  1. Rats kept awake for 2 weeks died
  2. Fatal Familial Insomnia (FFI) - insomnia that worsens until death; fatal after 6-30 months without sleep
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4
Q

EEG waves of different sleep states

A
  1. Relaxed wakefulness - Alpha waves
  2. Stage 1 - Theta waves
  3. Stage 2 - Sleep spindles, K-complex
  4. Stages 3/4 - Delta waves
  5. REM sleep - fast, random, sawtooth waves; similar to relaxed wakefulness!
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5
Q

How long are sleep cycles?

A

~90 min

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6
Q

place cells in sleep and memory replay (Diekelmann & Born, 2010)

A

Place cells in the hippocampus respond when an animal is in a specific location. In this study, recordings from 5 different place cells in the hippocampus were taken while rat runs in a triangle maze.

We see the same pattern of place cell firing when mouse runs a maze and when the mouse sleeps, as if they are replaying the experience while sleeping.

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7
Q

place cells

A

cells in the hippocampus that respond when an animal is in a specific location; in this manner, the hippocampus maps our spatial environment

Study shows that place cells have same pattern of firing when rat runs a maze and sleeps, indicating memory replay while sleeping.

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8
Q

effect of sleep on implicit skill learning task (Stickgold et al., 2001)

A

Individuals were presented with either a letter T or L in the periphery, and were asked to identify the letter. This study revealed that overnight interval between training and testing (i.e., one night’s sleep) led to significant improvement on the implicit skill learning task, and this skill improvement remained for many days.

Also revealed that lots of slow wave sleep (SWS) at the beginning of the night = more learning, and lots of REM sleep at the end of the night = more learning. I.e., SWS at beginning of night and REM at end is most impactful for learning.

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9
Q

How does type of sleep and when it occurs affect learning?

A

Stickgold et al., 2001, study of sleep and implicit skill learning task found that learning is maximized when:
1. Lots of slow wave sleep (SWS) at beginning of night
2. Lots of REM at end of night

No learning improvements when the opposite was seen.

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10
Q

memory engram model of how memory is encoded during sleep (systems consolidation of memory)

A

During slow wave sleep (SWS), the hippocampus recruits areas of the cortex to help replay recently encoded memories for consolidation purposes. In this situation, there is a recently encoded hippocampal part of a representation AND a recently encoded neocortical part of a representation. Think of this as “training” the cortex to encode memory on its own. This is known as “systems consolidation.”

During REM sleep, however, after memories are fully consolidated, the hippocampus is no longer involved, and memories are just encoded by the cortex. There are new synaptic connections between nodes in the cortex, and connections within nodes are strengthened. Think of this as the cortex (now independent from hippocampus) driving other areas of the cortex to permanentize the memory engram.

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11
Q

How do sleep spindles correlate with learning in infants?(Klinzing, Niethard & Born, 2019)

A

Babies were trained on a language learning task in which they were shown objects, and a certain word or name was played to help the baby learn the name of the object.

Infants who took a nap before testing showed an N400 EEG component in response to words that were incorrectly paired with objects, while infants who did not take a nap did not exhibit this effect, showing that only infants who took a nap developed object category representation (i.e., learned).

The reliability of the N400 peak was correlated with the power of sleep spindles during the nap. I.e., learning correlates to sleep spindles during nap.

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12
Q

How do sleep needs change with age?

A
  1. Newborns - 12-18hr sleep needs
  2. Infants - 14-15hr sleep needs
  3. Toddlers - 12-14hr sleep needs
  4. Preschoolers - 11-13hr sleep needs
  5. School-age children - 10-11hr sleep needs
  6. Teens - 8.5-9.25hr sleep needs
  7. Adults - 7-9hr sleep needs

Distribution of this sleep changes over development as well (e.g., napping)

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13
Q

sleep phase delay

A

12-21 year olds (adolescents) have a sleep phase delay, meaning they go to bed and wake up later (1-3h delay) than any other age group; this is a natural, biological phenomenon that is also visible in other mammalian species and is observed around the time of puberty

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14
Q

suprachiasmatic nucleus (SCN)

A

the SCN contains the “circadian pacemaker,” regulating the timing and consolidation of the sleep-wake cycle; the SCN is largely dictated by signaling from both light-entrainable oscillators in the retina, which provide light information, and food-entrainable oscillators in the gastrointestinal system, which provide information for when you should eat/sleep based on when you sleep/eat

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15
Q

light-entrainable oscillators

A

circadian clocks located in the retina that provide light information to the suprachiasmatic nucleus (SCN), helping to regulate the sleep-wake cycle

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16
Q

food-entrainable oscillators

A

circadian clocks located in the gastrointestinal system that indirectly provide information about food consumption to the suprachiasmatic nucleus (SCN), helping to regulate when you should eat/sleep based on when you sleep/eat

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17
Q

How does when we go to sleep change with age?

A

We go to sleep earlier when we are young, but ALL teenagers (whether night owls or not) exhibit sleep phase delay and go to bed later than the rest of the population. This sleep phase delay fades as we continue to age into the mid-late 20s and normalizes.

Also note that males tend to go to bed later than females.

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18
Q

How does when we go to sleep differ between males and females?

A

Males tend to go to sleep later than females from ages 10-40, but sleep times equalize from 40 onward

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19
Q

What is the effect of later school start times (i.e., more sleep) on academic achievement, daytime tiredness, behavioral persistence, and attitude? (Perkinson-Gloor et al., 2013)

A

A study in Switzerland found that school that started later (meaning 1+ extra hour of sleep) showed improved academic metrics in Math and German as well as improvements to daytime tiredness, behavioral persistence, and positive attitudes toward life.

In this manner, total sleep duration is a predictor of daytime tiredness (negative correlation), and daytime tiredness shows negative correlation with behavioral persistence, which has positive correlation to academic achievement and positive outlook on life.

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20
Q

How does lack of sleep affect driving?

A

Lack of sleep is heavily correlated with impaired driving skills and fatigue-related crashes…
1. Teen drivers who sleep less than 8 hours are 1/3 more likely to crash than those who sleep 8 or more hours
2. Lack of sleep reduces ability to process info, sustain attention, have accurate motor control, and react normally, all of which are crucial driving skills
3. Being awake for 18 hours is similar to BAC of 0.08, which is legally drunk

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21
Q

Who causes the majority of fatigue-related crashes?

A

Majority of fatigue-related crashes are caused by drivers under 25; this may be an indictment of school start times + sleep phase delay in adolescents

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22
Q

What is the prevalance of drowsy driving?

A
  1. At least 5% of adults admit to falling asleep at the wheel
  2. In 2017, 91,000 police-reported crashes involved drosy drivers
  3. In 2019, an estimated 697 fatal crashes involved drowsy driving
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23
Q

What is the impact of later school start times on car accidents? (Vorona et al., 2011)

A

Study comparing two high schools found that the school with the later start time resulted in fewer crashes among teen drivers both before school and after school compared to the school with the earlier start time. I.e., more sleep = less teen accidents

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24
Q

How prevalent are recommendations for later school start times?

A

As supported by a plethora of research…
1. Many prominent organizations such as The American Academy of Pediatrics and the CDC recommend that start times for middle and high school should be moved back
2. School districts worldwide are moving start times back to 8:30 or later

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25
Q

How does later school start time affect student sleep and student grades? (Dunster et al., 2018)

A

Study between two Seattle schools found that students who start school later got more sleep and performed better in first period classes

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26
Q

Socioeconomic status (SES) is a complex mixture of ____.

A

Complex mixture of:
1. Income level
2. Education level
3. Job prestige
4. Marital status

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27
Q

socioeconomic status (SES) as a predictor of future outcomes

A

SES is a strong predictor of life/educational outcomes such as vocab ability, school entry skills, graduation rates, and lifetime earnings

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28
Q

How have the black-white and rich-poor reading gaps changed over time? (Reardon, 2011)

A

Before segregation, there was a major gap in reading test scores between black and white children, but this gap has largely been closed.

However, as this gap closed, the reading gap between rich and poor children has been expanding steadily over time.

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29
Q

How has financial inequality changed over time? (Reardon, 2011)

A

The financial inequality gap has been increasing over time; there is a large gap between 50th percentile and 10th percentile income families, and an even larger gap between 90th percentile and 10th percentile.

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30
Q

How does SES correlate to school achievement? (Heckman, 2006)

A

kids enter school at age 6 with lower school abilities (worse grades) in the lower income quartiles than in higher income quartiles, and this trend continues throughout education, with low-income children continuously performing worse than high-income children

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31
Q

Is SES correlation to academic achievement a matter of “better schools?”

A

No! Middle-class students eligible for free lunch still scored better on math tests than low-income students in every school, even in the same classroom.

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32
Q

How does gray matter development differ across SES levels? (Hanson et al., 2013)

A

high SES children have greater development in total gray matter, frontal gray matter, and parietal gray matter than both mid SES and low SES children

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33
Q

How does parental education affect brain surface area? (Noble et al., 2015)

A

increased parental education is correlated with increased brain surface area, largely in temporal lobe and PFC; there is a linear increase in surface area for every 3 years of parental education

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34
Q

How does family income affect brain surface area? (Noble et al, 2015)

A

as family income increases, brain surface area increases, until about $50,000, then surface area minimally increases/plateaus as income further increases; specifically, there is a non-linear increase in brain surface area from $0-$50,000 family income

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35
Q

What brain regions exhibit functional differences on the basis of SES?

A
  1. Left perisylvian - language
  2. Anterior cingulate - cognitive control
  3. Medial temporal - declarative memory
  4. Lateral prefrontal - working memory
  5. Parietal - spatial cognition
  6. Occipito-temporal - visual cognition

Behavioral battery confirms this

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36
Q

What tests were conducted to analyze the left perisylvian/language system component of the SES behavioral battery? (Noble, McCandliss, and Farah, 2007)

A
  1. PPVT - experimenter says a word, child points to corresponding picture
  2. CTOPP - Blending words subtest (e.g., what word do the following sounds make?)

These collectively test high (semantic) and low (phenomic) aspects of language.

A correlation was found between this left perisylvian/language system and SES, and it was revealed that language skills mediate SES effects on cognitive conflict (ACC/cognitive control).

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37
Q

What tests were conducted to analyze the parietal/spatial cognition system component of the SES behavioral battery? (Noble, McCandliss, and Farah, 2007)

A
  1. NEPSY Arrows - 8 arrows point toward center, 2 of 8 point directly at the center dot, goal is to say which point at center dot and which don’t
  2. Mental Rotation - hands (L or R) presented at various orientations, goal is to say whether hands can be superimposed by rotating

A correlation was found between this parietal/spatial cognition system and SES.

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38
Q

What tests were conducted to analyze the medial temporal/declarative memory system component of the SES behavioral battery? (Noble, McCandliss, and Farah, 2007)

A
  1. NEPSY delayed memory for faces - children asked to say if image showed a boy or a girl, goal is to identify old faces after 20 min delay
  2. Incidental picture pair learning task - pairs of “Snodgrass” pictures shown, then 10 min delay, goal is to identify shown pair (out of 3)

A correlation was found between this medial temporal/declarative memory system and SES.

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39
Q

What tests were conducted to analyze the lateral prefrontal/working memory system component of the SES behavioral battery? (Noble, McCandliss, and Farah, 2007)

A
  1. Spatial working memory task
  2. Delayed non-match to sample - hold simple, nonverbalizable figural shape in memory; 4 sec study, 1 sec delay, ask if it matches

A correlation was found between this lateral prefrontal/working memory system and SES.

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40
Q

What tests were conducted to analyze the anterior cingulate/cognitive control system component of the SES behavioral battery? (Noble, McCandliss, and Farah, 2007)

A
  1. Go/no-go task - press button for all animals except the cat; 50 go, 10 no-go, measure failures to inhibit responses
  2. NEPSY auditory attention and response set - recorded words played at 1/sec, put red square in box when red is heard; phase 2 involves putting yellow for red, red for yellow, and blue for blue

A correlation was found between this anterior cingulate/cognitive control system and SES. It was also found that these SES effects on cognitive conflict are mediated by language skills.

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41
Q

What tests were conducted to analyze the orbitofrontal/reward processing system component of the SES behavioral battery? (Noble, McCandliss, and Farah, 2007)

A
  1. Reversal learning task - 2 decks of cards, 1 good, 1 bad, after successful learning the good and bad decks are switched; successful reversals are counted and measured
  2. Delay of gratification - noisy present wrapping with child’s back turned, measure time child avoids turning around

This orbitofrontal/reward processing system is the only cognitive domain of the behavioral battery in which NO correlation with SES was found.

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42
Q

How does SES affect different brain systems and their corresponding behaviors (SES behavioral battery)? (Noble, McCandliss, and Farah, 2007)

A

The SES behavioral battery was a study of 150 1st-grade children across SES levels that involved the conduction of multiple tests to analyze the effect of SES across six broad anatomical/cognitive domains:
1. Left perisylvian/language system
2. Parietal/spatial cognition system
3. Medial temporal/declarative memory system
4. Lateral prefrontal/working memory system
5. Anterior cingulate/cognitive control system
6. Orbitofrontal/reward processing system

This study ultimately found a correlation between SES and each of the cognitive domains except for orbitofrontal/reward processing, and also showed that SES effects on cognitive conflict were mediated by language skills, and that home and school environment modulated SES effects.

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43
Q

How do home and school environments modulate effects of SES on cognitive behavior (SES behavioral battery)? (Noble, McCandliss, and Farah, 2007)

A
  1. High performing supportive school offsets low parental education level
  2. Supportive, stable home environment offsets low family income
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44
Q

What is the hypothesized relationship as to how SES drives cognitive processes?

A
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45
Q

What are the effects of SES on early linguistic abilities? (Fernald et al., 2012)

A

Follow-up of 1995 study of “30 million word gap” found:
1. # of words spoken in home increases with SES
2. Accuracy of word knowledge increases with SES
3. Improved language processing speed correlated with SES
4. Grammatical complexity of speech increases with SES
5. Affirmations increase with SES

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46
Q

What is the “30 million word gap?”

A

derived from 1995 study, suggests that children up to age 4 from a lower socioeconomic status heard 30 million fewer words than children from a higher socioeconomic status

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47
Q

How are dendrites different in isolated vs. “enriched” environments?

A

isolated rats have decreased dendrite # and decreased dendrite complexity relative to rats in an “enriched” environment; the truth is that it’s not really the “enrichment” causing these effects, but rather the absence of an impoverished environment

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48
Q

What are the effects of chronic stress on the brain?

A

Heightened HPA axis activation that causes a sustained fight-or-flight response via the prolonged release of glucocorticoids (dangerous), leading to:
1. PFC atrophy
2. Hippocampus atrophy
3. Amygdala hypertrophy, and later atrophy

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49
Q

How do the neuronal effects of stress on dendrites change with age? (McEwen & Morrison, 2013)

A

Exposure to chronic stress causes dendritic shrinkage, and young animals are able to fully recover from this shrinkage, while recovery is blunted partially or completely in middle aged/aged animals. Dendrite count naturally decreases with age, however, so middle/old aged animals actually lose less dendrites than young (but still can’t recover).

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50
Q

How does SES impact emotion regulation and its neural substrates? (Kim et al., 2013)

A

Poverty was measured in 49 children at age 9, then at age 24, fMRI studies were conducted during an emotion regulation task.

It was revealed that low SES at age 9 correlates to low lateral PFC (amygdala) activity during emotion regulation at age 24 UNLESS took into account chronic stress.

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51
Q

What is significant about chronic stress with regard to SES?

A

chronic stress largely modulates effects of SES on the brain; e.g., in study of SES and emotion regulation, it was revealed that low SES at age 9 correlates to low lateral PFC (amygdala) activity during emotion regulation at age 24 UNLESS took into account chronic stress

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52
Q

How might environmental factors contribute to SES-related brain differences (environmental inequality)?

A

In certain situations, large amounts of neurotoxins may cause detriments to brain function. High-SES areas are able to fight pollution/prevent introduction of neurotoxins better than low-SES areas, which may help explain SES-related brain differences. This is known as environmental inequality, and environmental inequality correlates with SES on a state-by-state basis.

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53
Q

How does SES correlate with attention as shown by EEG? (Hackman & Farah, 2008)

A

Two unique stories were played in each ear, with visual cues indicating which story should be attended to.

In those with high maternal education (high SES), ERP shows smaller amplitude activity on the ignored side than the attended side. In those with low maternal education (low SES), however, there is less of a difference between attended and non-attended stimuli, suggesting that low SES correlates with reduced attention abilities.

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54
Q

What are the effects of family-based preschool programs on emotion and cognition? (Neville et al., 2013)

A

Study of three preschool interventions found that the PCMC-A family-based intervention had significant effects on parent emotion, child emotion, and child cognition (not as large an impact here) relative to child-based interventions, showing that supporting families and not just children is most effective.

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55
Q

What are the effects of family-based preschool programs on attention? (Neville et al., 2013)

A

Study of three preschool interventions found that a significant difference in ERP amplitude representing the attended side and nonattended side was present ONLY after PCMC-A family-based intervention (there was no difference in peaks prior to intervention), not in child-based interventions.

Given previous study showing worse attention in low-SES individuals, this may be applicable to low-SES children to improve attention. Also shows that supporting families and not just children is most effective.

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56
Q

How does preschool affect low-SES children? (Reynolds et al., 2011)

A

Review of 1970s Chicago study showed that preschool had strongest effect in those with lowest level of maternal education; i.e., preschool has greatest impact on low-SES children.

There was also a bigger impact in males than females.

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57
Q

Why do SES studies largely implicate maternal education?

A

mother’s education is the best predictor of educational ability

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58
Q

rate-of-return of preschool programs and invested capital discrepancy

A

preschool programs have the greatest rates of return to human capital investment, yet not a lot of money is invested into preschool programs; benefits-to-cost ratio of $8.74, meaning $1 investment returns $8.74

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59
Q

What is the effect of direct cash transfer (i.e., increasing SES) on baby brain development? (Troller-Renfree et al., 2022)

A

A study gave families monthly cash gifts in order to measure SES on baby brain development. This is a direct test of causality (randomized controlled trial) of SES on brain development and function, which is extremely challenging.

High-cash group showed greater EEG beta and gamma activity, which is correlated with future success.

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60
Q

Is the adolescent brain a “broken” or “defective” adult brain?

A

No! It is forged by evolution to have different features compared to children or adults

61
Q

4 adolescent behavioral changes in other social mammals

A
  1. Increased risk taking
  2. Increased sensation seeking
  3. Greater peer affiliation
  4. Greater exploratory range
62
Q

Which mental health disorders are adolescents more likely to be diagnosed with?

A
  1. Schizophrenia
  2. Depression
  3. Anxiety
  4. Substance abuse
  5. Eating disorders
63
Q

structural brain differences in adolescents vs. adults

A
  1. Prefrontal regions not fully developed, but limbic system is
  2. Increased dopamine
  3. Decreased gray matter (cell bodies)
  4. Increased white matter (axon tracts/connectivity)
64
Q

How do dendrites change with age?

A

as soon as we reach puberty, dendritic spikes experience a massive decrease due to synaptic pruning

65
Q

dorsolateral PFC (DLPFC) vs. ventromedial PFC (VMPFC) in higher order cognition

A

DLPFC important for executive control, i.e., cool cognition
VMPFC important for emotional processing, i.e., hot cognition

66
Q

“Cool” vs. “Hot” cognitive control

A
  1. Cool pertains to the lab, hot pertains to life
  2. Cool is alone, hot is in groups
  3. Cool is hypothetical, hot involves real situations
  4. Cool is low arousal, hot is high arousal
67
Q

How do “cool” and “hot” executive functions develop with age?

A

Psychosocial maturity (“hot” cognitive control) develops toward the end of adolescence, while intellectual ability (“cool” cognitive control) begins to rapidly develop around 15-16 years of age

68
Q

What drives adolescent decision making?

A

Adolescent decision making does not depend on risk perception, as teens know they shouldn’t participate in “risky” decisions. Rather, it heavily relies on:
1. Reward sensitivity
- seeking high levels of novelty and stimulation to achieve same subjective feeling of pleasure, related to puberty and depends on limbic system (which is already fully developed)
2. Self regulation
- peer influence
- Future orientation
- Emotional arousal

69
Q

How does the development of limbic regions and prefrontal regions differ?

A

Limbic regions develop much faster/sooner than PFC regions (generally almost done by start of adolescence), which explains much of the adolescent decision making differences

70
Q

What is unique about the reward system during adolescence?

A

Increased reward sensitivity because ventral striatum is much more active during adolescence; this greater reward circuitry activation —> cravings for reward heightened and fulfilled by social media, gaming, etc. This is confirmed via fMRI.

71
Q

What is the Iowa and Cambridge Gambling Task, and what does it reveal?

A

Volunteer draws card from 1 of 4 decks, winning/losing money each time with a goal to make as much money as possible. There are 2 “good” decks and 2 “bad” decks, and a monitoring device shows that the body registers which decks are good and bad befire the conscious mind (literally like a hunch/gut feeling).

Moreover, as the number of bets increases, there is a lot of activity in the VMPFC.

72
Q

correlation between inhibitory control (SSRT) task and Iowa Gambling Task

A

Good stoppers in SSRT might take less time to decide which Iowa decks are “good” and which are “bad”

73
Q

What is the stop-signal reaction time (SSRT) task, and what does it measure?

A

Stop-signal reaction time (SSRT) is an inhibitory control task that is similar to go/no-go task, and shows that increased stop-signal reaction time = slower inhibitory response

74
Q

How is the “cool” vs. “hot” go/no-go task unique in teens?

A

teens are much more likely to “go” on a happy face “no-go” stimuli (i.e., more false alarms), correlating with the increased ventral striatum reward activity that is present in adolescents

75
Q

What is the effect of peer influence on risky decision making in adolescents? (Chein et al., 2011 in Blakemore & Robbins, 2012)

A

In the driving simulator/fMRI study, adolescents make more risky decisions in the presence of their peers, correlating to an increase in ventral striatum activity.

76
Q

What is the effect of parent influence on risky decision making in adolescents? (Guassi Moreira & Telzer, 2018)

A

In the driving simulator/fMRI study, adolescents were less likely to make risky decisions in presence of mother vs. random adult, correlating to a decrease in ventral striatum activity in presence of mother compared to random adult.

77
Q

4 divisions of the social brain

A
  1. Mentalizing
  2. Reward
  3. Mirror neuron
  4. Emotional salience
78
Q

neural basis of the mentalizing system

A
  1. Temporoparietal junction
  2. Superior temporal sulcus
  3. Precuneus/posterior cingulate
  4. Dorsal medial PFC (DMPFC)
  5. VMPFC
79
Q

neural basis of the reward system

A
  1. Orbitofrontal cortex
  2. Ventral striatum
  3. VMPFC
  4. Anterior cingulate
  5. Putamen
  6. Caudate
80
Q

neural basis of mirror neuron system

A
  1. Superior parietal lobe
  2. Inferior parietal lobe/intraparietal sulcus
  3. Superior temporal sulcus
  4. Dorsal premotor
  5. Ventral premotor/inferior frontal
81
Q

neural basis of emotional salience system

A
  1. Posterior cingulate
  2. Orbitofrontal cortex
  3. Dorsal anterior cingulate
  4. Insula
82
Q

right fusiform face area (FFA)

A

BOLD activity in the right FFA goes up for faces and down for objects, showing right FFA is specialized for facial recognition; however, facial perception is beyond the FFA, more like a facial recognition network that is heavily reliant on amygdala-fusiform connectivity…the amygdala “trains” the FFA, and we become more reliant on the fusiform areas for facial recognition with age

83
Q

Does facial perception solely rely on the right FFA?

A

facial perception is actually beyond the right FFA, as we also see activation in other areas of the brain in response to faces…more like a facial recognition network that is heavily reliant on amygdala-fusiform connectivity.

In children, the amygdala “trains” other regions, including FFA, in a long developmental process. This connectivity doesn’t go away with age, but we begin to predominantly rely on fusiform areas for facial perception with age.

84
Q

How soon in development can we recognize faces? (Morton & Johnson, 1991)

A

1991 study analyzing look time shows that by 19 weeks old, babies can distinguish faces from other objects

85
Q

What is significant about amygdala-fusiform connectivity?

A

There is strong connectivity between the amygdala and the fusiform areas, allowing for facial recognition; likely also involved in emotional association with faces.

The amygdala “trains” other regions to become category selective, including FFA, in a long developmental process. This connectivity doesn’t go away with age, but we begin to predominantly rely on fusiform areas for facial perception with age.

86
Q

How does amygdala-fusiform connectivity change with age?

A

this high level of connectivity doesn’t go away with age, but we begin to predominantly rely on fusiform areas for facial perception with age

87
Q

How does category selectivity develop with age?

A

Children don’t yet have particular areas of the brain that preferentially respond more to e.g., faces than to any other object…no category selectivity yet, amygdala drives category selectivity with age

88
Q

facial perception in children

A

Children don’t yet have one particular area of the brain that preferentially responds more to faces than any other object (no real FFA), indicating that children use a wide network of regions for facial perception…the amygdala “trains” other regions, including FFA, in a long developmental process

89
Q

What brain regions are active when watching biological motion?

A

fMRI shows that the STS (mirror neuron system) and amygdala are active in response to biological motion but not scrambled, nonhuman-like motion

90
Q

mirror neuron system (MNS)

A

neurons that are similarly active…
1. While performing goal-oriented movement
2. While watching/imaging movement

Mirror neurons found in monkeys, hard to prove in humans.

Shows that premotor areas not just for planning movement but also for understanding movement in others.

91
Q

What dictates level of mirror neuron activity (dancer study)? (Calvo-Merino et al., 2005)

A

Study of dancers showed that for best mirror neuron activity, subject must be familiar with that type of movement. Specifically, dancers had more MNS activity than non-dancers, and ballet dancers had more MNS activity than other dancers during ballet dance, while other dancers had more MNS activity than ballet dancers during other dances.

92
Q

2 theories of mirror neuron system (MNS) development

A
  1. Innately specified
    - evidence is that social interactions are highly conserved across species and are essential fo social interaction
    - mimicking behavior suggests automatic matching
  2. Purely associative learning
    - human infants receive sensorimotor experience to support MNS
    - we can modify MNS responses with experience even in adults
93
Q

How is the mirror neuron system (MNS) related to empathy?

A

there is similar activity during pain and observed pain in the anterior cingulate (ACC) and right insula, which are mirror neuron areas

94
Q

Theory of Mind (TOM)

A

concept that somebody else has an internal knowledge different than your own; TOM is often tested using a variant of the false belief task, such as Sally-Anne test, Smarties test, or Marble test

In these studies, pointing/eye-gaze is more sensitive than verbal report.

95
Q

When does Theory of Mind (TOM) develop?

A

Often tested using a variant of the false belief task, revealed that false belief understanding (i.e., TOM) develops around age 4-5; however, environmental factors (e.g., # of siblings) may drive earlier developmental shift

In these studies, pointing/eye-gaze is more sensitive than verbal report.

96
Q

neural basis of Theory of Mind (TOM)

A

medial prefrontal cortex (mPFC)

97
Q

prevalence of Autism Spectrum Disorder (ASD)

A
  1. 1 in 44 children diagnosed in 2022 (2.27%)
  2. Prevalence rate of 6/1000, or 0.6%
  3. 4-5 times more likely in boys than girls

This increase in diagnoses is related to more awareness, changing categorization (e.g., “mental retardation” decrease, Asperger’s now form of ASD) rather than an actual increase in prevalence.

98
Q

What explains the increase in Autism Spectrum Disorder (ASD) diagnoses?

A

ASD has a prevalence rate of 6/1000, or 0.6%, but 1/44 children, or 2.27%, were diagnosed in 2022.

This increase in diagnoses is related to more awareness, changing categorization (e.g., “mental retardation” decrease, Asperger’s now form of ASD) rather than an actual increase in prevalence. Some evidence that increase in prevalence is real (like increasing paternal age), but not as much as driven by diagnosis.

99
Q

How has autism terminology evolved?

A

historically “autistic,” but now there is a shift to “person first” (e.g., person with autism) or “identity first” (e.g., autistic person) among different groups

100
Q

core symptoms of Autism Spectrum Disorder (ASD)

A

There is a web of correlations to ASD with regard to biomarkers, comorbidities, and genetics, but the core symptoms of ASD include:
1. Impaired social communication/interaction
2. Restricted/repetitive behavior

101
Q

What is unique about the “spectrum” of Autism Spectrum Disorder (ASD)?

A

the “spectrum” of ASD is highly variable and not necessarily “linear”

102
Q

neural differences of Autism Spectrum Disorder (ASD)

A

There is global brain overgrowth in ASD; specifically, there is a larger amount of gray matter in children with autism, corresponding to a larger head

It is theorized that this is due to lack of sufficient synaptic pruning.

103
Q

What is the broken mirror hypothesis, and what studies give rise to it?

A

Theory that ASD is caused by deficits in the MNS, based on the following studies:
1. An EEG study shows that in controls, rest phase synchronous activity goes down most during movement, but also while watching movement. In ASD, however, rest phase synchronous activity goes down only during movement.
2. The higher the score on autism symptom indices, the lower the neural activity in MNS during facial expression task.

Is difference in MNS actually causing ASD? Likely to be broader issue driving BOTH ASD and deficits in MNS.

One paper states that review of 25 studies presents evidence that deficient MNS probably does NOT lie at core of autism.

104
Q

How is face responsiveness altered in Autism Spectrum Disorder (ASD)?

A

Reduced face responsiveness is the most widely replicated finding in ASD; differences are present in early stages of face processing (FFA), but differences may not be restricted to these regions.

105
Q

eye tracking as a predictor of Autism Spectrum Disorder (ASD)

A

Eye tracking at 2-6 months acts as a predictor of ASD: children with ASD show high eye fixation that decreases with age, while neurotypical children have lower eye fixation that ramps up then flatlines with age.

High risk siblings (having sibling w/ autism) w/o symptoms show similar trend to neurotypical children, while high risk siblings w/ symptoms but no diagnosis show slightly similar trend to ASD but not as extreme.

106
Q

social motivation hypothesis of Autism Spectrum Disorder (ASD)

A

infants usually find looking at faces to be highly rewarding, and those who do not will spend less time looking at faces and potentially miss important social skill development during critical periods…this leads to issue of causality: Is lack of eye fixation & social reward the cause of ASD or another result from broader functional differences?

107
Q

early amygdala dysfunction hypothesis of Autism Spectrum Disorder (ASD)

A

Early amygdala dysfunction has been hypothesized to drive social and cognitive impairments that are seen in ASD, including mirror neuron differences (broken mirror hypothesis), low social motivation (social motivation hypothesis), etc., leading many to believe that early amygdala dysfunction completely underlies ASD.

108
Q

evidence for critical periods in occipital development of kitten

A

taping one eye shut leads to permanent lack of occipital development in kitten if “window” of critical/sensitive period closes; development can only occur within the particular window

109
Q

When do most sensitive periods occur?

A

generally early in development, prior to formal K-12 schooling

110
Q

How do concreteness and abstractness relate to sensitive periods?

A

The more concrete/less abstract the cognitive process ability (e.g., vision vs. peer social skills), the sharper the drop in plasticity at the end of the sensitive period.

On the other hand, abstract and social processes retain significant plasticity for much of lifespan.

111
Q

When does mass synaptic pruning occur in the frontal, visual, and auditory cortexes?

A

synaptic density of auditory cortex and frontal cortex decreases at ~ 4 years old (also 15.5 for frontal), and that of visual cortex decreases at ~ 8 months old

112
Q

evidence of adult plasticity in taxi drivers

A

Taxi driver study of plasticity shows that increased time as taxi driver is correlated with increased gray matter volume in the posterior hippocampus, suggesting adult plasticity.

113
Q

Hebbian model of long-term potentiation (LTP)

A

Donald Hebb proposed the idea that “neurons that fire together, wire together,” or that the more two neurons tend to fire at the same-ish time, the stronger connections will become, forming a network. This is a model of LTP, or synaptic plasticity, which persists into adulthood.

114
Q

evidence of long-term depression (LTD) in sea slug (Eric Kandel & LTD in Aplysia californica)

A

Eric Kandel found that repeated stimulation of Aplysia californica siphon led to eventual stoppage of gill withdrawal (which is what typically occurs when siphon is stimulated), indicating learning. Specifically, sensory neuron response does not change, but motor neuron response decreases despite the fact that input remains the same.

This proves LTD, or the weakening of synaptic connectivity between sensory and motor neuron.

115
Q

How is lifelong plasticity evident in the somatosensory cortex? (Jenkins et al., 1990)

A

The homunculus somatosensory map can change as a result of experience.

For example, study of monkeys showed that areas of somatotopic map representing the fingers expanded as a result of experience, even in adults.

116
Q

How is plasticity evident in string instrument players? (Elbert et al., 1995)

A

Study of string instrument players used MEG to show larger magnetic field in right regions of the brain (corresponding to left arm/hand/fingers) in string players that started earlier in life than those who started later in life and than controls; those who started later in life still had larger field than controls.

117
Q

How is plasticity evident in the brain through juggling? (Draganski et al., 2004)

A

Study of juggling showed that people assigned to juggle for 6 weeks had increased gray matter in motion perception regions, even weeks after juggling ended.

118
Q

From a neural perspective, what is unique about reading braille and spoken language in the blind?

A

fMRI shows that the visual areas of the brain have largely been “taken over” by Braille reading and spoken language in the blind, with the visual cortex activating in response to both Braille reading and spoken language. This is visible in both those who became blind early in life and those who became blind later in life, exhibiting lifelong plasticity in the brains of the blind.

Moreover, study shows that the VWFA activates in response to reading Braille words, but not nonsense Braille.

119
Q

From a neural perspective, what is unique about lip reading in the deaf?

A

fMRI shows that the auditory speech areas of the brain have largely been “taken over” by lip reading in the deaf, with the auditory cortex activating in response to lip reading. This exhibits plasticity in the brains of the deaf.

120
Q

How does learning to use tools modify brain function and exhibit plasticity? (Maravita & Iriki, 2004)

A

Expanded tool-use in monkeys leads to expansion of neural representation for “reachable space” in parietal cortex.

121
Q

What is BDNF, and how does it relate to exercise?

A

BDNF is a growth factor that helps LTP persist and helps neurons survive.

Exercise produces BDNF, and BDNF levels in hippocampus correlate to learning and memory associated with exercise regimen.

122
Q

How does exercise relate to academic achievement in children? (Hillman et al., 2008)

A

Study shows that increased aerobic capacity (meaning cardiovascular training) is correlated with increased math and reading performance; note that this study does not investigate strength training

123
Q

How does exercise affect cognition? (Hillman et al., 2008)

A

Randomly assigning aged adults to exercise or control group shows that exercise has a large effect size on cognition. This impact remains large at all ages, and shows that exercise may protect against age-related cognitive decline.

124
Q

How does retirement relate to cognitive decline? (Andel et al., 2016)

A

Study shows that retirement is often a “turning point” that kicks off cognitive decline, including decline in memory and cognitive speed; people who have high cognitive demand jobs and leisure activities (i.e., demanding exercise) have better cognitive abilities even before retirement and are able to better maintain it after retirement (though it still decreases).

125
Q

How is plasticity evident in musicians?

A

Musicians have an enlarged auditory cortex, and size correlates to years of practice.

126
Q

4 ways in which cognitive theories use neuroscience data, and examples of each (Willingham & Lloyd, 2007)

A
  1. Direct Observation of Internal Representations
    - E.g., humans and Macaques have cells that preferentially respond to a particular number = representation of number in the brain
  2. The Reality of Cognitive Constructs
    - Localization helps demonstrate reality of phonological deficit. E.g., we see differences in the brains of typically reading children and dyslexic children, but interventions can lead to remediation that exhibits neurotypical-like brain activity
  3. Separate Systems for Apparently Unitary Functions
    - E.g., breakdown of memory; there are different types of memory with different neural representations, despite the apparent unitary function of memory…e.g., STM and LTM represented in different tasks and have different corresponding brain activation, like different systems
  4. Reliable Knowledge of Brain Guides Cognitive Theory
    - Before brain imaging, psychologists couldn’t agree if mental imagery was based on images or built upon linguistic representations! Studies show that visual areas are active during mental imagery, and this correlates with imagining size as well, with a larger part of occipital cortex active for larger objects (i.e., we use reliable knowledge of the brain to guide this idea that mental imagery is true imagery in the brain)…also, language regions seem uninvolved. Moreover, mental imagery has category selectivity, with mental imagery of faces and places corresponding to FFA and PPA activation, respectively.
127
Q

What is significant about the shared mechanisms of attention and working memory (WM)?

A

The shared mechanisms of attention and WM exhibits the idea that the two might be more or less integrated; the overlap is so significant that maybe we should view them as “hand-in-hand” rather than separate systems when doing research.

128
Q

What does it mean when an educational product is “Brain-Based?”

A

“Brain-Based” is used in educational spaces for marketing purposes. Brain-Based material can refer to:
1. Brain-based educational theory
- e.g., Universal Design for Learning
2. Brain-based principles and corresponding instructional techniques
3. Brain-based neurofeedback training
4. Brain-based educational products

This is problematic because these products are purely for marketing and often have no evidence or loosely based evidence behind them. This is why we have the 4 alternatives and the 5-step plan for assessing these products (see other slides).

129
Q

4 alternatives for labeling and assessing “brain-based” products

A
  1. Brain supported
    - evidence from neuroscience supports behavioral intervention
  2. Brain derived
    - intervention derived from neuroscience data and theories
  3. Brain driven
    - manipulate brain activity directly to change behavior (e.g., smart drugs, tDCS)
  4. Brain inspired
    - most current products (e.g., Lumosity), based more or less loosely on brain data and theories
130
Q

5 steps to evaluate brain based educational products

A
  1. Goals
    - identify educational goals
  2. Match
    - determine if there is a match between goals and purpose of brain based product
  3. Research
    - evaluate the merits of the brain based rationale and research supporting the product
  4. Pros and cons
    - identify the benefits and limitations of the product and consider alternatives
  5. Impact on behavior
    - characterize the impact of the product on behavioral performance
131
Q

What Works Clearinghouse

A

website that gathers data regarding “brain based” products, compiling research to inform consumers of the effectiveness of a given product

132
Q

4 broad categorical directions for the future of educational neuroscience

A
  1. Direct brain stimulation
    - e.g., TMS, tDCS
  2. Smart drugs
  3. Genetic testing of all children
  4. Increase in use of existing technology
    - specifically fNIRS
133
Q

What is transcranial magnetic stimulation (TMS), and what is it used for?

A

Creates “temporary lesion” by using magnetic flux to induce current in the brain, permitting manipulation of cortical activity; can be single pulse or repetitive (rTMS), and is used for:
1. Mood disorder via rTMS
2. Single session TMS can temporarily silence brain region for experimental purposes
3. FDA approved for treatment of depression

134
Q

single pulse transcranial magnetic stimulation (TMS)

A

induces transient change in excitability, can excite or inhibit; typically used during a task and useful to establish chronology of cortical processing

135
Q

repetitive transcranial magnetic stimulation (rTMS)

A
  • low frequency (~1 Hz) inhibits cortical function
  • high frequency excites cortical function
136
Q

What is transcranial direct current stimulaton (tDCS), and is it effective?

A

Can be bought on Amazon and uses electrodes on scalp with low current to stimulate neurons.

It is not FDA regulated, and there is no evidence of it working to improve cognitive function in healthy people (i.e., probably not effective outside of lab setting).

However, it has been shown to improve motor function in stroke survivors.

137
Q

What are smart drugs, and are they effective?

A

Smart drugs consist of taking off-label medications such as Ritalin, Adderall, and other stimulants with the intention of “supercharging” cognition.

Smart drugs have no real evidence of cognitive effects in neurotypical people (but they’re like caffeine), BUT they improve attitude toward work you are doing…i.e., heavily placebo-dependent.

138
Q

What is genomic education?

A

In the future, as genomic analysis cost decreases and the human genome becomes more well known, we may be able to perform genetic testing on ALL children, allowing us to implement personalized, genomic-based education that is literally tailored to each person’s genome.

This has major (ethical) concerns:
1. Environment also plays major role…not just genes!
2. Could give rise to major discrimination in schools, jobs, etc.

139
Q

What is functional near-infrared spectroscopy (fNIRS), and what are its advantages and disavantages?

A

fNIRS has cap with optodes that emit/detect near infrared light onto the head…it is sensitive to differences in oxy- and deoxyhemoglobin (same as BOLD) signal, allowing for measurement of brain activity. This should become more refined in the future and is thought of as one future of educational neuroscience.

Advantages:
1. Small, portable, non-invasive
2. Less-sensitive to motion than MRI

Disadvantages:
1. Only a small number of sensor locations
2. Cannot image deep tissues (like EEG)

140
Q

study of EEG brain synchrony in the classroom (Dikker et al., 2017)

A

Study of EEG in the classroom shows how brain activity changes during different activities. This study saught to measure brain synchrony between students and teacher to analyze learning outcomes (e.g., if one child is less in sync, does that equal less learning, etc.).

141
Q

Why do we need infrastructure for the future of MBE?

A

There are so many obstacles in the way (e.g., neuromyths, ethics, brain-based education, learning styles, etc.). Moreover, we need people to work hand-in-hand! Can’t have teachers and researchers working separately yet try to reach educational neuroscience goals.

142
Q

4 wishes of MBE infrastructure to aid educational neuroscience

A
  1. Research schools
  2. Creating a new generation of interdisciplinary researchers
    - educational researchers who are specially trained and experts in learning and teaching
  3. Large-scale databases of learning/development
  4. Designs informed by neuroscience and genetics
143
Q

What is needed to actually establish MBE infrastructure?

A
  1. Teachers/administrators need to become more familiar with research methods
  2. Researchers need to become more familiar with real-world school settings and concerns
144
Q

What is a research/laboratory school?

A

elementary or secondary school operated in association with a university, college, or other teacher education institution and used for educational research, …integrates science and education, a literal direct bridge that many propose as infrastructure for the future of educational neuroscience.

Follows the model of medicine = teaching, research, & clinical duties overlap.

Laboratory School at UChicago is still operational, and IMBES is working to create a network of these schools.

145
Q

analogy of education with medicine

A

Doctors used to have many methods to treat the sick, but little info why they worked, or they didn’t work at all…however, this changed with the advent of evidence-based medicine, and we have gotten stricter with training and doctor compensation and respect has increased. As medicine has developed in this manner, life expectancy has increased.

We could do this with education!

Today, teachers have many methods for teaching, but little infor why they worked, or if they work at all…however, education can become an evidence-based field to similarly improve education and thereby improve society.

146
Q

short-term predictions if analogy of education with medicine is realized

A
  1. May provide additional insight into why methods that work do work
  2. Improvement will be numerous and of small size (few magic bullets)
  3. Most important findings likely to be broad
147
Q

long-term predictions if analogy of education with medicine is realized

A
  1. Placebo effects in education?
  2. Possible negative findings/conclusions
    - not everything will be as learnable as hoped
    - individual differences may decrease as education is optimized
    - full genotyping?
  3. Training of teachers will change in many of the same ways that training of doctors changed
148
Q

What is the proposed new generation of interdisciplinary researchers that will aid the future of educational neuroscience?

A

We need to create a new generation of interdisciplinary researchers that focus on science/education hand-in-hand in order to build an effective bridge.