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Biological Psychology > Bio Psych Exam 3 > Flashcards

Bio Psych Exam 3 Flashcards

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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

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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

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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)

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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.

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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

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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

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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
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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
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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
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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)
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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

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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
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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

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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

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15
Q

What neurotransmitter is most at play in the mesolimbic pathway?

A

dopamine

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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

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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
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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)
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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…

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20
Q

How do we diagnose mental disorders?

A

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

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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)

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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
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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
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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

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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
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26
Q

What is meant by proximate vs. ultimate explanations?

A
  • proximate: mechanisms and developmental history
  • ultimate: adaptive function and phylogenetic history
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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

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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

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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
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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)

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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)

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