Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biological Psychology > Bio Psych Exam 3 > Flashcards

Bio Psych Exam 3 Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Psychology flashcards Psychology 101 flashcards GRE® Psychology flashcards
1
Q

What qualifies as a drug?

A

An (1) exogenous chemical (2) not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body when (3) taken in relatively low doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are pharmacokinetics vs. pharmacodynamics?

A

Pharmacokinetics refers to what the body does with the drug, whereas pharmacodynamics refer to what the drug does to the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do different routes of administration impact pharmacokinetics?

A

Impact how high you feel and the length of the high (in the cocaine example)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the blood brain barrier? Why do we care about it?

A

Barrier that restricts the indiscriminate access of certain substances in the bloodstream to the CNS. We care about it because it protects our brain from unwanted substances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is tolerance?

A

A decrease in the effectiveness of a drug that is administered repeatedly
- once someone has developed tolerance, they will likely show withdrawal symptoms if they suddenly stop taking the drug
- decrease in effectiveness of binding, receptors become less sensitive, or receptors decrease in overall numbers, coupling can be less effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is sensitization?

A

An increase in the effectiveness of a drug that is administered repeatedly
- ex: movement effects of cocaine show sensitization whereas the euphoric effects don’t show sensitization, maybe even tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do drugs interact with receptors?

A
  • can be specific, reversible
  • may activate or inactive a receptor
  • may increase or decrease a particular cell function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the difference between agonist and antagonist?

A
  • agonists are drugs that help the system by enhancing, mimicking, or facilitating the effects of an NT on the postsynaptic cell
  • antagonists are drugs that hurt/stifle the system by opposing or inhibiting the effects of a neurotransmitter on the postsynaptic cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is competitive vs. noncompetitive binding?

A
  • competitive is there is only one site for the NT or drug to bind
  • noncompetitive is there is more than one site for the NT or drug to bind
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 5 classes of medications and give examples from each?

A
  • Antidepressants: used to lift mood out of a depressive episode (SSRIs, SNRIs, NDRIs, MAOIs)
  • Mood stabilizers: used to regulate mood so that it doesn’t get too low or too high (lithium, anticonvulsants, atypical antipsychotics)
  • Anti-anxiety medications (SSRI, SNRI, anticonvulsants, benzodiazepines)
  • Stimulants (adderall, ritalin)
  • Anti-psychotics (typical antipsychotics, atypical antipsychotics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are SSRIs mechanism of action?

A

prevents the reuptake of serotonin, leave the NT in the synapse longer so that it has more time to bind to the postsynaptic cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between an antidepressant and a mood stabilizer?

A
  • mood stabilizers try to keep you at the neutral, baseline level
  • antidepressant tries to bring you up to the baseline level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do positive and negative reinforcement play a role in the development and sustaining of substance abuse disorder?

A

reinforcement learning enables organisms to adjust their behavior in order to maximize rewards
- positive reinforcement: a positive consequence with increase behavior, so the rapid euphoria you feel after taking a drug will increase drug taking behavior –> establish addiction
- negative reinforcement: a response/behavior is strengthened by removing/avoiding the aversive thing, so the feeling of alleviated pain after drug taking will increase drug taking behavior –> physiological changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the mesolimbic pathway and why do we care?

A

transports dopamine from the VTA to the nucleus accumbent and amygdala
- it is important for the positive reinforcing effects of both natural rewards and drugs of abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What neurotransmitter is most at play in the mesolimbic pathway?

A

dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are withdrawal symptoms?

A

physical and psychological behavior displayed by an addict when drug use ends
- i.e., insomnia, tremors, anxiety, depression, irritability, cravings, irregular heartbeats, seizures, hallucinations, convulsions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the want/like theory of addiction?

A
  • wanting = some salient incentive from the environment; form of motivation; cues
  • liking = actual pleasurable impact of the reward consumption; fragile
  • the wanting dopaminergic systems become hyper-reactive; there’s an increase in wanting over time due to sensitization of the mesolimbic pathway
  • liking of the drug stays the same or even decreases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some of the risk factors for addiction?

A
  • older adults are more likely to abuse certain styles of drugs
  • genetic makeup
  • environment: Adverse Childhood Experiences (ACEs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are ACEs?

A

Adverse Childhood Experiences: early life stressors –> acute/dynamic epigenetic effects (short term effects) –> adapted/maladapted neuronal networks (long-term adaptations) –> behavioral outcome
- ACEs include physical abuse, parental substance abuse, and many more that impact…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do we diagnose mental disorders?

A

use the DSM-5; basically a checklist with criteria outlining mental disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are your feelings on how we diagnose mental disorders?

A

makes it more “clear-cut” than mental disorders actually are; also, each individual’s journey with mental illness is unique, whereas the DSM-5 is overgeneralized and very westernized
- however, it is a decent attempt to define mental disorders so that there is a common understanding amongst people who diagnose (standardization principle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the serotonin hypothesis of depression?

A
  • drugs that blocked the reuptake of monoamines (especially serotonin) helped people who have depression
  • therefore, we inferred that there must be low levels of these neurotransmitters (especially serotonin)
  • WRONG! There is no evidence to suggest that low levels of NT cause depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the neurotrophic hypothesis of depression?

A
  • neurotrophic = related to growth/survival of neurons
  • increased serotonin and NE activity at certain synapses leads to important downstream actions which may underlie the observed antidepressant effect –> downregulation (decreased response and/or decrease number of or sensitivity of receptors) of post-synaptic receptors –> transcription of BDNF (brain-derived neurotrophic factor; involved in plasticity for learning and memory)
    HYPOTHESIS: When under certain stress conditions, we see cell death. One hypothesis is that antidepressants work via reversal of these changes seen under stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is meant by “consilience”?

A

conceptual integration; sciences and areas of study build on one another, from the most fundamental units to trying to understand the world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What did Dr. Bergstrom mean when describing the mind as a black box, a sponge, or a blank slate?

A
  • black box: behaviorism knew there is a brain but didn’t want to mess with the details; just want to know what goes in and out –> a blank slate brain would be as useful as a hard drive without software: it may have potential and capacity, but without software to enable the learning, a computer (or brain) won’t do anything
  • blank slate: psychology suggested the world has no “pre-programming”
  • sponge: we soak up things in our environment; if a sponge learned indiscriminately, it would fail to recognize that some things are more important to learn than others, thus scarcely improving upon the blank slate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is meant by proximate vs. ultimate explanations?

A
  • proximate: mechanisms and developmental history
  • ultimate: adaptive function and phylogenetic history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Is it possible that a mild, non-clinical form of “depression” may have had some evolutionary value?

A

yes; negative emotions may not feel good, but their motivational power may lie precisely in our desire to alleviate them
- depression may have had “survival value” as a social-emotional hibernation that allowed humans to: conserve energy, avoid conflicts and other risks, let go of unattainable goals, take time to contemplate, and signal to others the need for assistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Can you relate the end of Dr. Bergstrom’s talk to our previous discussion of the neurotrophic hypothesis of depression?

A

BDNF regulates the differentiation of neurons during development, promotes the survival and growth of axons, dendrites, neurons throughout life
- it is vital to the brain’s job of adapting to a changing world
- BDNF functions to translate activity into synaptic and nerve plasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some natural next steps scientists could take to improve treatment of depression, given what we’ve discussed in terms of the serotonin hypothesis and the neurotrophic hypothesis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a biorhythm? Can you give some examples?

A

natural rhythm in behavior or a bodily process
- circannual: yearly (migratory cycles of birds)
- infradian: more than a day (human menstrual cycle)
- circadian: daily (human sleep/wake cycle)
- ultradian: less than a day (human eating cycles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the circadian rhythm? Can you give some examples?

A

a biorhythm whose time frame is a day-long (human wake/sleep cycle, pulse, blood pressure, body temperature, alertness, feeding behavior)

32
Q

What is meant by exogenous vs. endogenous?

A

exogenous: cues from the outside; endogenous: cues from the internal (we must have a biological clock: a neural system that times behavior by producing the biorhythms)

33
Q

What is the retinohypothalamic pathway?

A

takes light information to the SCN to tell us how to behavior depending on the light/dark cycle

34
Q

Retinohypothalamic pathway

A
  1. light enters eye
  2. activates melanopsin receptor in retina (RGCs)
  3. Travels to SCN in hypothalamus
  4. SCN sends info to areas which regulate sleep and wakefulness (orexin neurons; ventrolateral pre optic area)
35
Q

Where does the retinohypothalamic pathway start and end?

A

retinal ganglion cells (RGCs) to the suprachiasmatic nucleus

36
Q

Where is our “master” clock located?

A

on top of the optic chiasm

37
Q

What is meant by the term “master” clock?

A

suprachiasmatic nucleus of the hypothalamus (SCN)
- daily rhythms observed in firing rate of cells
- ticking based on cycle of protein production/inhibition
- exerts control by direct synaptic connections with other regions and secreting neuromodulators (like melatonin)

38
Q

What are the different stages of sleep?

A
  • N1: alpha decreases, slow rolling eye movements, motor activity slightly reduced, partial awareness of surroundings
  • N2: eye movements rare, not much motor movement, some bursts of waves, sleeping soundly
  • N3: high voltage slow waves, eye movements are rare, not much motor movement
  • REM: EEG reverts to a mix of beta and theta, bursts of eye movements, muscle paralysis
39
Q

How long do we sleep?

A

about 8 hours a day, meaning we spend about 2 hours in REM

40
Q

What is the cycle of sleep?

A

N1, N2, N3, REM
- we tend to sleep in 90-110 minute periods
- NREM happens sooner
- REM happens around the end of the 90-minute period

41
Q

What are the differences between n-sleep and r-sleep?

A
  • N-sleep: large range of activities; dreaming occurs but not as vividly as in R-sleep; sleepwalking, talking, and night terrors are more common; talking or grinding teeth; flailing, banging an arm, kicking a foot; maintain muscle posture
  • R-sleep: atonia (no muscle tone, everything is very still); mechanisms that regulate body temperature stop working; vivid dreams
42
Q

How would you know if someone was in n-sleep versus r-sleep?

A

based on atonia of muscles, eye movement, respiration rate, etc.

43
Q

Describe the mutual inhibition effects of the “flip flop” switch in VLPOA

A
  • if we are active in the brain stem, meaning we are awake and alert, we inhibit the VLPOA –> cannot send as many inhibitory signals back to the brain stem
  • if sleep-promoting region in VLPOA is activated, it promotes sleep by sending inhibitory signals to the brain stem and inhibit arousal systems –> can’t send back as many inhibitory signals
44
Q

Why do you sleep?

A
  • energy conservation
  • restorative
  • learning and memory
45
Q

What is narcolepsy?

A

slow-wave sleep disorder in which a person uncontrollably falls asleep at inappropriate times

46
Q

What is REM sleep behavior disorder?

A
  • physically act out vivid, often unpleasant dreams
  • no atonia of muscles
  • maybe brainstem lesions?
  • mostly male
  • seems to be linked to Parkinson’s and other neurodegenerative disorders, but it is unclear why
47
Q

What is actigraphy?

A
  • watch like device worn for two consecutive weeks to try to understand habitual sleep patterns
  • generates sleep and wake estimates from movement
  • used to assess sleep and circadian features
48
Q

What are the pros of actigraphy?

A
  • can be helpful for assessing circadian rhythm disorders and getting an overall understanding of one’s sleep patterns
49
Q

What are the cons of actigraphy?

A
  • tends to overestimate when the individual is awake
  • has not been validated for measuring sleep stages
50
Q

What is the relationship between social disadvantage and the brain structure of neonates?

A

social disadvantage during pregnancy is associated with smaller brain volumes at birth

51
Q

Are social disadvantages and the brain structure of neonates directly related or are they mediated by anything?

A

mediated by maternal chronodisruption

52
Q

Why might social disadvantage lead to chronodisruptions?

A
53
Q

How does sleep seem to operate in relation to depression? Is it a cause? Is it a symptom? Is it separate?

A

Cyclical relationship; not able to determine directionality –> better to consider them as separate things that could temporally relate to one another

54
Q

Is depression only seen in adults?

A

NO; age-adjusted manifestations of depression symptoms

55
Q

What are some challenges in helping children with depression?

A

difficult to detect; ex: externalizing behaviors versus internalizing behaviors as a kid make it difficult to differentiate if they are experiencing depressive symptoms or other behavioral issues

56
Q

Should we only pay attention to objective measures of sleep?

A

No

57
Q

How do subjective measures play a role in sleep?

A

Maybe help understand how effective individuals’ sleep patterns are based on emotions and behaviors when sleep is disrupted/irregular

58
Q

Do sleep disturbances predict childhood depression or does childhood depression predict sleep disturbances?

A

sleep disturbances predict childhood depression

59
Q

How might our previous discussion of ACEs relate to sleep disturbances?

A
60
Q

What is the difference between measurement and manipulation?

A
  • measurement: brain activity is measured during a task with the aim of identifying brain areas that might be involved in the performance of that task
  • manipulation: the structure or function of the brain is altered, and the resulting effects on behavior are observed
61
Q

What is the BOLD signal?

A

blood oxygenation level-dependent signal
- an indirect measure on neural activity that is used in fMRIs
- when neurons fire, they require additional oxygen
- BOLD relies on the different magnetic properties of oxygenated and deoxygenated blood
- increased neural activity –> increased blood flow to replenish the area –> surplus of oxygenated blood –> increase in the BOLD signal –> this is known as the hemodynamic response function

62
Q

What is meant by spatial resolution and temporal resolution?

A
  • spatial resolution refers to the capacity a technique has to tell you exactly which area of the brain is active
  • temporal resolution describes a technique’s ability to tell you exactly when the activation happened
63
Q

Manipulation techniques

A
  • lesion studies
  • brain stimulation (including DBS, TMS, and ECoG)
  • optogenetics
64
Q

Measurement techniques

A
  • electrical activity (including cellular recordings, EEG, ECoG, and MEG)
  • functional brain imaging (PET, fMRI)
  • structural methods (CT/CAT, MRI)
65
Q

Lesion studies

A
  • manipulation technique
  • guiding question: if a brain region is damaged, what functions remain and which ones become impaired?
  • assumes that the function of a brain area can be inferred from the behaviors that can no longer be performed after the area is damaged
  • problems: sham lesions (in animals); other non-relevant issues (in humans); non-specific/diffuse damage; cortical reorganization; was the behavior very localized to begin with?
66
Q

Deep brain stimulation (DBS)

A
  • manipulation technique
  • electrode is neurosurgically implanted; helpful for Parkinson’s Disease and OCD
  • problems: usual surgery risks (especially increasing with age); what happens if placement isn’t exactly perfect?
67
Q

Transcranial magnetic stimulation (TMS)

A
  • manipulation technique
  • place a coil over a particular area; current passes through, causes cortical cells to depolarize
  • noninvasive, clinically useful for depression
  • problems: how localized is it really; makes interpretation difficult; reproducibility issues; safety
68
Q

Optogenetics

A
  • manipulation technique
  • mice are genetically engineered to express membrane channels that are light-sensitive
  • problems: cells are responding to light, but not how they would “normally”; trying to get more precision for subtypes of neurons; not at the human level (maybe not supposed to be?)
69
Q

Cellular recordings

A
  • measurement technique
  • intracellular recording: tiny electrodes inserted directly inside a neuron to record their electrical selectivity
  • extracellular recording: tiny electrodes inserted into the fluid surrounding neurons to record electrical current generated by the neuron in the electrode’s vicinity
  • …
70
Q

Electroencephalography (EEG)

A
  • measurement technique
  • put electrodes on scalp to record “brain waves” –> measuring the summed graded potentials from thousands of neurons
  • the flow of ions causes distortions of the electrical field
  • really good temporal resolution
  • problems: can be hard to figure out where exactly these electrical signals came from (poor spatial resolution); the skull distorts signals
71
Q

Electrocorticography (ECoG)

A
  • intracranial EEG
  • for research purposes, often paired with some form of stimulation (manipulation!) –> can be both manipulation and measurement technique
72
Q

Magnetoencephalography (MEG)

A
  • measurement technique
  • very similar to EEG, but magnetic waves are not distorted by the skull
  • usually laid on top of high-resolution MRI
  • better spatial resolution, but you need to shield out any other magnetic fields, including the Earth’s magnetic field and requires liquid helium to cool some of the sensors
73
Q

Positron emission tomography (PET)

A
  • measurement technique
  • different radioactive agents can be used with biomarkers of disorders and pathologies
  • tracers can also label chemicals (like neurotransmitters) and other things to assess function
  • lack of structure in PET scans, so usually overlaid to make it more comprehensive
  • good for studying because it shows task-related activations as well as brain metabolism and neurochemistry
  • problems: lower spatial resolution; slower temporal resolution (tracer needs to be washed out)
74
Q

Functional magnetic resonance imaging (fMRI)

A
  • measurement technique
  • non-invasive
  • high spatial and temporal resolution
  • most often measures the blood oxygenation level-dependent (BOLD) signal
75
Q

Computerized tomography (CT/CAT)

A
  • measurement technique
  • rotates an x-ray around the patient’s head
  • faster and cheaper than MRI, but lower resolution
  • can be used in situations where magnets cannot (i.e., implanted metal devices)
76
Q

Magnetic resonance imaging (MRI)

A
  • measurement technique
  • shows brain structure
  • bone shown but CT is better
  • cortical thickness
  • problems for MRI and fMRI: movement matters; who are we scanning?; statistical woes; very expensive

Biological Psychology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions