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Biopsychology > Biopsychology Exam 3 > Flashcards

Biopsychology Exam 3 Flashcards

1
Q

What are 5 things necessary for a drug to be a drug?

A
  1. must be exogenous
  2. must be not necessary
  3. must be able to be given in relatively low doses
  4. must have an effect
  5. must have a site of action
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2
Q

What does it mean for a drug to have a site of action?

A

The locations at which molecules of drugs interact with molecules locatedon or in cells of the body, thus affecting some biochemical processes of these cells

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3
Q

What is pharmacokinetics

A

what the body does with the drug

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4
Q

what is pharmacodynamics

A

what the drug does to the body

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5
Q

The understanding and use of pharmacokinetic
principles can

A

increase the probability of therapeutic success and reduce the occurrence of adverse drug effects in the body

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6
Q

Routes of Drug Adminastration

A

Intravenous (IV) injection — into a vein
* Intraperitoneal (IP) injection — into space surrounding stomach, liver etc.; esp animals
* Intramuscular injection (IM) — COVID, flu vaccines
* Subcutaneous injection (SC) — into the space beneath the skin
* Orally — swallow pill
* Sublingual — under the tongue
* Inhalation — smoked
* Intranasal — snort
* Topical — into skin

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7
Q

Which routes of adminastration are quick

A

IV and smoking

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8
Q

What are two ways that Cyclobenzaprine can be given?

A

Can be given via swallowing a pill or sublingual oral dose (dissolving under tongue)

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9
Q

Is swallowing an oral dose or a siblingual oral dose quicker?

A

Sublingual is much quicker because they travel through capillaries of mouth and right to brain and not through stomach

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10
Q

After absorption, the drug distributes to

A

interstitial and intracellular fluids

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11
Q

Which organs recieve most of the drug

A

Liver, kidneys, brain, and other well-irrigated organs

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12
Q

Is the drug release to muscles and fat tissue slow or fast?

A

slow

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13
Q

What is the blood brain barrier

A

Barrier that restricts the indiscriminate access of certain
substances in the bloodstream to the CNS

Layer of astrocytes that prevents substances in the
circulating blood from freely entering the extracellular fluid
of the brain (i.e., blocks things from passing through
capillaries in the brain)

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14
Q

There’s a lack of the blood brain barrier in

A

Pituitary gland
Pineal gland (day/night cycle)
Area postrema (vomit toxic substances)

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15
Q

Metabolism Definition

A

Set of reactions and transformations that drugs undergo in the body

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16
Q

Excretion Definition

A

Elimination by the body of residues of drug metabolism.

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17
Q

what is the most important excretory organ

A

kidney

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18
Q

Excretion Pathways

A

Renal (kidneys)
Biliary (bile) and fecal
Pulmonary (lungs)
Sweat, saliva and tears
Breast milk

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19
Q

what is the margin of safety between

A

the dose response curve for the analgesic effect and the dose response curve for the depressive effect

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20
Q

Tolerance Definition

A

A decrease in the effectiveness of a drug that is administered repeatedly

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21
Q

Once someone has developed a tolerance, they will likely show ____ if they stop taking the drug suddenly

A

withdrawal symptoms

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22
Q

How is tolerance associated with receptors and binding?

A
  • decrease in effectiveness of binding
  • receptors become less sensitive
  • receptors decrease in overall numbers
  • coupling can become less effective
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23
Q

Sensitization definition

A

An increase in the effectiveness of a drug that is administered repeatedly

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24
Q

Is sensitization or tolerance more common?

A

tolerance

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25
Q

How can cocaine show both tolerance and sensitization?

A

movement effects are sensitization

euphoric effects are tolerance

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26
Q

2 categories of drugs

A

antagonists and agonists

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27
Q

Agonist definition

A

A drug that mimics or facilitates the effects of a neurotransmitter on the postsynaptic cell

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28
Q

Antagonist definition

A

A drug that opposes or inhibits the effects of a neurotransmitter on the postsynaptic cell

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29
Q

Two different types of binding

A

competitive and non-competitive binding

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30
Q

Competitive binding definition

A

when the receptor only has one site and either the neurotransmitter or the drug will get there first

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31
Q

non-competitive binding definition

A

when there are two receptor sites and both the neurotransmitter and the drug can bind
BUT two neurotransmitters could bind and two drugs could bind

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32
Q

If the drug serves as a precursor would it be an agonist or antagonist?

A

agonist

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33
Q

If the prevents storage of NT in vesicles, would it be an agonist or antagonist?

A

antagonist

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34
Q

If the drug inhibits release of NT, would it be an agonist or antagonist?

A

antagonist

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35
Q

If the drug stimulates postsynaptic receptors, would it be an agonist or antagonist?

A

agonist

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36
Q

If the drug stimulates autoreceptors, would it be an agonist or antagonist?

A

antagonist

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37
Q

If the drug blocks autoreceptots, would it be an agonist or antagonist?

A

agonists

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38
Q

If the drug inactivates acetylcholinestaerase, would it be an agonist or antagonist?

A

agonist

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39
Q

3 types of small molecules

A

Acetylcholine, Amines, Amino Acids

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40
Q

3 types of catecholamines

A

Dopamine, Norepinephrine, Epinephrine,

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41
Q

What is serotonin involved with

A

Mood, aggression, respiration, appetite

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42
Q

Which Neurotransmitters are really important for learning and memory?

A

Glutamate and GABA

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43
Q

5 Types of Medications

A
  1. Antidepressants
  2. Mood stabilizers
  3. Anti-anxiety medications
  4. Stimulants
  5. Anti-psychotics
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44
Q

Antidepressants are used to

A

LIFT mood out of a depressive episode

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44
Q

Besides depression, what are anti depressants used for?

A

Anxiety Disorders
OCD
Panic Disorders
Phobias
Bulimia
PTSD

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45
Q

is loss of energy an example of reduced positive affect or increased negative affect

A

reduced positive affect

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46
Q

Is serotonin dysfunction associated with increased negative affect or reduced positive affect?

A

increased negative affect

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47
Q

Is dopamine dysfunction associated with increased negative affect or reduced positive affect?

A

decreased positive affect

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48
Q

5 types of anti-depressants

A

SSRIs
SNRIs
NDRIs
MAOIs
Tricyclis

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49
Q

What is the difference between antidepressants and mood stablizers?

A

Antidepressants are used to LIFT
mood out of a depressive episode

Mood stabilizers are used to
REGULATE mood so that it
doesn’t get too low (depression)
or too high (mania)

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50
Q

3 types of Mood Stablizers

A

Lithium
Anticonvulsants (anti-epileptic)
Atypical antipsychotics

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51
Q
A
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51
Q

What is lithium helpful for?

A

mechanism of action isn’t quite known; effective for manic
episodes & maintaining remission; helpful for suicide prevention

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52
Q

What are anticonvulsants helpful for

A

uncertain mechanism of action; effective
for acute manic phases of bipolar disorder; inconclusive for bipolar
depression; a tonnnnnn of side effects

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53
Q

Types of Anti-anxiety medications

A

SSRIs
SNRIs
Anticonvulsants
Benzodiazepines

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54
Q

Characteristics of Benzodiazepines

A

Depressants/sedatives — feelings of calm, drowsiness, etc.

Generally these are GABA agonists

Inhibits arousal systems

People tolerate this well, but there is a real risk of dependence, abuse, and
withdrawal reactions

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55
Q

What are Xanax, Valium, and Ativan all examples of?

A

Benzodiazepines

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56
Q

What should Benzodiazapines not be taken with?

A

Alcohol

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57
Q

What does Aderall do?

A

It blocks the reuptake of norepinephrine and dopamine

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58
Q

What does Ritalin do?

A

non-competitively blocks the reuptake of dopamine and noradrenaline

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59
Q

What is psychosis?

A

A condition where people lose touch with reality

Thoughts/perceptions are disturbed

Hard to tell what is real and what is not real

Delusions & hallucinations

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60
Q

What are some characteristics of Typical Antipsychotics?

A
  • “First generation”; 1950s
  • Generally, these are blocking
    dopamine at D2 receptors; tight
    binding
  • They are still useful and prescribed
    out of desperation
  • High risk of side effects
  • Haldol & Thorazine
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61
Q

What are some characteristics of Atypical Antipsychotics?

A

*“Second generation”; 1990s
* Generally, these are blocking
dopamine at D2 receptors; loose
binding
* Very useful!
* Side effects not as bad as typical
antipsychotics
* Risperdal, Olanzapine

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62
Q

What is the order of operations for drug administration?

A

alcohol/stimulant/substance abuse –> mood disorders –> anxiety disorders –> ADHD –> nicotine dependance

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63
Q

What makes something a substance abuse disorder?

A
  • Compulsion to seek out and take the drug (escalation)
  • Impaired control in limiting intake
  • Persistent despite very clear evidence of overtly harmful consequences
  • Progressive neglect of alternative pleasures or interests
  • [Relapse]
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64
Q

What is an example of negative reinforcement with drug use?

A

Feeling of alleviated pain after drug taking will increase drug taking behavior

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65
Q

What type of reinforcement typically establishes an addiction?

A

positive reinforcement

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65
Q

Where does positive reinforcement take place?

A

Synaptic
strengthening in
the ventral
tegmental area
* Sits next to the
substantia nigra; also
dopaminergic
* Mesolimbic
pathway (from VTA
to ventral striatum)

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66
Q

What is the ventral striatum involved with?

A

Initial stages of
addictive
behaviors

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67
Q

What is the dorsal striatum involved with?

A

Habit formation;
cue-induced

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68
Q

Negative Reinforcement Definiton

A

Negative reinforcement is when a
response/behavior is strengthened by
removing/avoiding the aversive thing

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69
Q

What is wanting in terms of drug abuse?

A

some salient incentive; form of motivation; CUES

The wanting dopaminergic systems becomes hyper-reactive; there’s an increase in wanting over time due to sensitization of mesolimbic pathway

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70
Q

What is liking in terms of drug use?

A

actual pleasurable impact of the reward consumption; fragile

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71
Q

Does the liking of a drug increase with time?

A

no it typically stays the same or even decreases

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72
Q

What are 3 risk factors of Addiction

A

Age, Genetics, Environment

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73
Q

Neurological disorders definition

A

Neurological disorders are “…diseases of the central and peripheral nervous
system. In other words, the brain, spinal cord, cranial nerves, peripheral
nerves, nerve roots, autonomic nervous system, neuromuscular junction, and
muscles

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74
Q

Mental Disorders are

A

Mental disorders are “…generally characterized by a combination of abnormal thoughts, perceptions, emotions, behavior and relationships with others

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75
Q

What do psychologists use to diagnose things?

A

DSM-5

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76
Q

What are the pros of the checkbox approach?

A

“Measuring the invisible”
Standardization
Can help rule things out

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77
Q

What are the cons of the checkbox approach?

A
  • maybe we’re measuring wrong
  • different clinical presentation earns the same diagnosis
  • is it actually helpful for understanding the disorder
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78
Q

What is trephination?

A

drill holes into the skull; release “evil spirits”; 7,000-10,000
years old!

79
Q

How did psychologists use Isolation and asylums for mental disorders?

A

remove the person with mental illness from their families/
society; supposed to get treatment there but there wasn’t much in the way of treatment; often brutal and cruel methods were used and living conditions were
unacceptable

80
Q

What is electroconvulsive therapy?

A

one disease could cure another; seizure could cure psychiatric illness; method became more efficient and more widely adopted in the 1940’s

81
Q

Symptoms of Depression

A
  • depressed mood
  • anhedonia
  • feelings of worthlessness or guilt
  • suicidal ideation, plan, or attempt
  • fatigue or loss of energy
  • increased or decreased sleep
  • extreme weight gain or loss
  • decreased ability to think or concentrate, indecisiveness
  • agitation
82
Q

How did they treat depression in the 1930s?

A

benzedrine was marketed as a treatment for fatigue and mild
depression-like symptoms (not depression)

83
Q

How did they treat depression in the 1940s?

A

ECT

84
Q

How did they treat depression in the 1950s?

A

drugs for anxiety came out, but it didn’t really help with depression

85
Q

How did they treat depression in the late 1950s?

A

first drugs that do seem to treat depression (a happy accident;
intended to treat tuberculosis); worked by inhibiting monoamine oxidase
(MAO) —> ultimately blocked reuptake of 5-HT & NE

86
Q

What is the Serotonin Hypothesis of Depression?

A

Drugs that blocked the reuptake of monoamines (esp. 5-HT) helped people (and continue to help) who have depression

86
Q

Do low levels of neurotransmitters cause depression?

A

nope

87
Q

Neurotrophic Hypothesis

A

Increased 5-HT and NE activity at certain synapses leads to important downstream actions which may underlie the observed antidepressant effect

88
Q

What is the downregulation of post-synaptic receptors?

A

decreased response and/or decrease number of or sensitivity of receptors

89
Q

Definition of Transcription

A

the process by which a cell makes an RNA copy of a piece of DNA. This
RNA copy, called messenger RNA (mRNA), carries the genetic information needed to make proteins in a cell

90
Q

BDNF

A

brain-derived neurotrophic factor; involved in plasticity for learning & memory

91
Q

How do psychiatrists make decisions (4 Steps)?

A

Step 1: get a diagnosis
Step 2: Choose a drug based on prior response to other drugs, safety,
family history if applicable, patient choice. SSRI’s usually tried first because they are generally well-tolerated
Step 3: choose a low dose and slowly ramp up
Step 4: adequate trial is at least 6 weeks at a therapeutic dose

92
Q

Consilience Defintion

A

agreement between the approaches to a topic of different academic subjects, especially science and the humanities

93
Q

3 Options for the Mind

A

Blank Slate, Black Box, Sponge

94
Q

What is the difference between a proximate explanation and an ultimate explanation

A

Put briefly, ultimate explanations are concerned with why a behavior exists, and proximate explanations are concerned with how it works.

94
Q

Tinbergen’s Four Whys

A

The immediate influence of behavior (proximate)

Developmental influences (proximate)

Function (or adaptive purpose)

Evolutionary origins (ultimate cause)

95
Q

What is the proximate explanation for why children resist going to bed?

A

Being in the dark increases heart rate, respiration, and levels of anxiety (“afraid” of the dark)

96
Q

What is the ultimate explanation for why children resist going to bed?

A

Those who avoided being in the dark alone did a better job of surviving long enough to reproduce

97
Q

Why is pregnancy sickness a medical mystery?

A

Consistent pattern of symptoms:
 Starts ~2-4 weeks / Stops ~14 weeks
 Not just “morning sickness”
 Unusual appetite sensitivity
 Unusual scent sensitivity
 Cross-cultural prevalence
 Pregnancy sickness incurs costs:
 Diminished calorie intake
 Slower digestion = slower absorption of nutrients
 Nausea = lower productivity / efficiency

98
Q

Which types of food might contain teratogens

A

vegetables, meat, fried food

99
Q

what is the embryonic period of maximum vulnerability

A

beginning around 3 weeks after conception to around the end of first semester

100
Q

When does pregnancy sickness end?

A

PS ends completely (~14wks) when the
nutritional needs of the fetus outweigh any
additional protection by PS (economic)

101
Q

How would The immediate influence of behavior (proximate cause) explain pregnancy sickness?

A

physiological changes corresponding to pregnancy trigger a recalibration of bodily systems that regulate nausea

102
Q

How do developmental influences (proximate cause) explain pregnancy sickness?

A

This system is not designed for childhood; it
is developmentally linked to puberty & pregnancy

103
Q

How does function or adaptive purpose (ultimate cause) explain pregnancy sickness?

A

To protect the developing fetus from environmental dangers

104
Q

How does the evolutionary origins (ultimate cause) explain pregnancy sickness?

A

The adaptation probably reflects a small modification of already existing “nausea regulation” to serve the specific needs
of fetus protection during the earliest stage of pregnancy

105
Q

How does the brain change with depression?

A

Severe or prolonged depression associated w/ reduced size of hippocampus, frontal lobe (OFC), ACC +

Changes in the synapses of the nucleus accumbens (near the caudate and putamen) make it less responsive to reward

hyperactive amygdala

106
Q

What is the evolutionary perspective on depression?

A

Depression, in its non-disordered, milder form, may have had
“survival value” as a
social-emotional hibernation

107
Q

How could depression be helpful evolutionarily?

A

the hibernation may help conserve energy, avoid conflicts and other risks, let go of unattainable goals, take time to contemplate, and signal to others the need for assistance

108
Q

3 ways that evolved mechanisms can fail:

A
  1. mechanism can fail to become activated when the relevant adaptive problem is confronted (ex. seeing a snake but not reacting)
  2. mechanism can become actived in inappropriate contexts (ex. sexually attracted to relatives)
  3. the mechanism can fail to coordinate with other mechanisms (ex. even if you like a mate you might not devote mating effort to being with them)
109
Q

What might play a role in the dysregulation of various evolved systems?

A

the mismatch of ancestral and modern environments

110
Q

What is the neurotransmitter theory?

A

Depression is caused by the lack of seratonin

111
Q

Is the neurotransmitter theory for depression true?

A

No, because serotonin levels are not lower in people with depression, the 5HT receptor is not more active in people with depression, SERT is not more active in people with depression, and larger doses of SSRIS do not produce larger effects

AND antidepressants don’t work right away, antidepressant drugs are all about equally effective, drugs + psychotherapy product better outcomes, and relapse is more common when drugs are used without psychotherapy so it cannot just be about the lack of serotonin

112
Q

What changes in the brain are caused by traditional antidepressants?

A

increased neurogenesis (new neurons are formed) in the hippocampus, increased dendritic branching, increases of BDNF that support neuron survival and synaptic connectivity

113
Q

What is an approach to explaining how anti-deprresants work in combination with psychotherpay?

A

anti-depressants create a “window of opportunity” whereby we have the cellular means to think, feel, and behave differently,
and the enhanced plasticity to strengthen those changes to support recovery and resilience. That is: we can re- orient ourselves to life events/circumstances and chart a new (e.g., meaningful, sustainable) path forward

114
Q

What does BDNF do?

A

it regulated differentiation of neurons during development, promotes the survival and growth of axons, dendrites, and neurons throughout life

summary: BDNF translates activity into synaptic and nerve plasticity

115
Q

What are circannual rhythyms and what is an example of them?

A

Yearly – migratory cycles of birds

116
Q

What are infradian rhythyms and what is an example of them?

A

more than a day and human menstrual cycle

117
Q

What are circadian rhythyms and what is an example of them?

A

daily and human sleep-wake cycles

118
Q

What are ultradian rhythyms and what is an example of them?

A

less than a day – human eating cycles

119
Q

As opposed to nocturnal, humans are ____

A

diurnal

120
Q

Besides for sleep, what else falls under circadian rhythyms?

A

Pulse, blood pressure, body temperature, alertness, feeding behavior and
more

121
Q

Are biological clocks endogenous or exogenous

A

endogenous

122
Q

What is the biological clock?

A

The neural system that times behavior by producing the biorhythms

123
Q

What happend when an experimenter but people in a bunker for a month?

A

People’s circadian rhythyms shifted late r

124
Q

What does the biological clock help with?

A

Synchronizes behavior to the passage of a real day & makes predictions
about tomorrow, Anticipating of events, prepare for them physiologically & cognitively, regulating feeding times, sleeping times, etc

125
Q

What can impact our circadian rhythyms?

A

light pollution (from phones), Jet Lag

126
Q

Is it harder to go from East to West or West to East

A

West to East

127
Q

Where is the master clock located?

A

The suprachiasmatic Nucleus of the Hypothalamus (SCN)

128
Q

What is the arousal/wakefulness pathway

A

RGCs –> suprachiasmatic Nucleus –> Orexin neurons (lateral hypothalamus)

129
Q

What is the sleep promoting pathway?

A

RGCs –> suprachiasmatic Nucleus –> Ventrolateral Preoptic Area

130
Q

What is the retinohypothalamic pathway?

A

RGCs–> SCN –> hypothalamus –> thalamus –> pituitary –> autonomic neurons in spinal cord…

131
Q

What is the special photopigment in ganglion cells?

A

Melanopsin

132
Q

How does relevant information travel to the SCN

A

the retinohypothalamic pathway

133
Q

How are the daily rhythyms of the SCN observed?

A

the firing rate of cells and the ticking is based on cycle of protein producing/inhibition

134
Q

How does SCN exert control

A

direct synaptic connections with other regions and secreting neuromodulators (like melatonin)

135
Q

When does the brain experience alpha waves?

A

during rest and relaxation

136
Q

when does the brain experience during beta waves?

A

when alert, attentive, and thinking

137
Q

What happens during N1

A

Alpha decreases, slow rolling eye movements,
motor activity slightly reduced, partial awareness of
surroundings

138
Q

WHat happens during N2

A

eye movements rare, not much motor
movement, some bursts of waves, sleeping soundly

139
Q

What happens during N3

A

high voltage slow waves, eye
movements rare, not much motor movement

140
Q

What happens during REM

A

EEG reverts to mix of beta & theta, bursts of eye movements, muscle paralysis

141
Q

How long is a typical sleep cycle

A

90 minutes

142
Q

How long does a typical adult spend in REM each night

A

~2 hours

143
Q

How many cycles does a typical adult go through every night

A

5-6

144
Q

How does sleep change over the lifespan

A

we get different amounts of REM sleep at different ages

145
Q

What type of activities happen during N-sleep

A

decrease in body temperature, increase in growth hormone release, sleep talking, sleep walking, night terrors, talking or grinding teeth, flailing, maintaining muscle posture

146
Q

Atonia Definition and when does it occur

A

No muscle tone; condition of complete muscle inactivity produced as sleep regions of the brainstem inhibit motor neurons and during R-sleep

147
Q

What is the body temperature during R sleep

A

close to room temperature

148
Q

when do nightmares occur

A

N-sleep

149
Q

what type of neurons are in the VLPOA

A

GABAergic neurons (inhibitory)

150
Q

Why do we sleep?

A

Energy conservation, restorative, learning and memory

151
Q

How does energy conservation explain why we sleep?

A

Reduce a person’s energy demand during part of the day/night when it’s least
efficient to hunt for food + our body has decreased metabolism during sleep

152
Q

How does restoration explain why we need sleep?

A

Sleep lets the body repair and replete cellular components necessary for
biological functions that become depleted throughout an awake day

153
Q

How does the rat study explain learning and memory’s connection to sleep?

A

the rats showed the same brain activity pattern while doing the task and while sleeping.

154
Q

Narcolepsy

A

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

155
Q

Cataplexy Definition

A

sudden loss of muscle tone; slurred speech, weakness etc; often triggered by a strong emotion

156
Q

Sleep Paralysis Definition

A

temporary inability to move or speak while falling asleep or upon waking; can remember these events

157
Q

Hypnagogic Hallucinations definition

A

particularly vivid and frightening because you may not be fully asleep when
you begin dreaming and you experience your dreams as reality

158
Q

What are some features of narcolepsy?

A

Low orexin/hypocretin and Genetic - 20-40x higher with family member with narcolepsy

159
Q

What is REM Sleep Behavior Disorder

A

Physically act out vivid, often unpleasant dreams –> sleep talking, shouting, screaming, hitting, punching etc.

no atonia of muscles

160
Q

What are some features of REM Sleep Behavior Disorder

A

Maybe due to brainstem lesions

Mostly male

Seems to be linked to Parkinson’s and other neurodegenerative disorders, but
it’s unclear why

161
Q

Why is sleep so important for young children?

A
  • Maintaining homeostasis
    -Promoting system critically and plasticity
    -Consolidation of memory and learning
162
Q

What are sleep disturbances associated with?

A
  • Poorer immune functioning
  • Increased risk for obesity
  • Worsened cognitive abilities
  • Increased risk for psychopathology
163
Q

What is Actigraphy?

A

A method of measuring sleep that is worn typically for two consecutive weeks, in the form of a watch, and uses to generate sleep and wake estimates from movement and circadian features

164
Q

What changes do pregnant women have in terms of sleep?

A
  • earlier sleep timing
  • changes in activity patterns
  • poorer sleep quality
  • shifts in hormones which might be related to sleep
165
Q

What is some evidence that maternal circadian rhythms affect the fetus?

A

Maternal melatonin and glucocorticoids can cross
placenta to access fetal tissue

166
Q

Can you describe the relationship between social disadvantage and the brain structure of neonates? Are they directly related or are they mediated by anything?

A

They are mediated by sleep – Sleep is a potential mediator: Sleep is the mechanism in which social disadvantage impacts neonatal brain volumes
For the babies and their neonatal brain structure, greater irregularity in mother’s brain sleep schedule and later bedtime was associated with less cortical folding, gray and white matter, and smaller infant brain volumes

167
Q

Can you think of reasons for why social disadvantage might lead to chronodisruptions?

A

Irregular work schedules, exposure to noise, light, non-ideal sleep environments

168
Q

What is the difference between Manipulation and Measuring Techniques

A

Manipulation techniques involve the structure or function of the brain being altered the resulting effects on behavior are observed

Measuring techniques involve brain activity being measured during a task and looking at the behavior associated during that task and

169
Q

What are the problems with Lesion Studies?

A

Brain could be reorganized
We don’t know if the function was localized to begin with
May be nonspecific damage
Control conditions?
In humans - other non-relevant issues
In animals - sham lesions

170
Q

What are the 3 manipulation tactics?

A

Lesions, Brain Stimulation, Optopgenetics

171
Q

What are 2 types of Brain Stimulation?

A

DBS and TMS

172
Q

What is DBS?

A

Electrode neurosurgically implanted
Treatment option for parkinsions and OCD
Not used for research only

173
Q

What are the problems with DBS

A

Usual surgery risks which increase with age
What if the placement isn’t exactly perfect

174
Q

What is TMS?

A

Place a coil over a particular area
Current passed through skull and causes depolarization in populations of neurons
Non-invasive
Clinically useful for depression

175
Q

What are the problems with TMS

A

Not fully localized
Reproducibility issues
Makes interpretation quite difficult
Safety issues!

176
Q

What is the assumption of lesion studies

A

Function of a brain area can be inferred from the behaviors that can no
longer be performed after the area is damaged

177
Q

What is optogenetics?

A

Mice are genetically engineered to express membrane channels that are light sensitive
Light-triggered
Can insert these proteins into particular areas, then apply light
The photoreceptors will act like they do in the eyes
Invaluable for understanding neural circuitry
Brain has no pain receptors so it doesn’t hurt the mouse
More focused than TMS

178
Q

What are the problems with optogenetics?

A

Cells are responding to light, but now how the would normally respond
Trying to get precision for subtypes of neurons
Not at the human level

179
Q

What are the 3 Main categories for measurement?

A
  1. Electrical Activity
  2. Functional Brain Imaging
  3. Structural Methods
180
Q

What is the difference between Intracellular Recording and Extracellular Recording?

A

Tiny electrodes inserted directly inside a neuron to record their electrical selectivity

Tiny electrodes inserted into the fluid surrounding neurons to record electrical currents
generated by the neuron in the electrode’s vicinity

181
Q

How does an EEG work?

A

Put electrodes on scale to record brain waves
Measuring the summed graded potential from thousands of neurons
Some of these waves are rhythmical
Records thousands of neurons at a time
The flow of ions cause distortions of the electrical field
Really great temporal resolution (milliseconds)
ERPs
This is EEG that is synchronized with a task

182
Q

What are the problems with EEG

A

Skull distorts electrical activity
Can be hard to figure out where exactly these electrical signals came from

183
Q

Which two methods of measuring electrical activity do not have the skull problem?

A

ECoG and MEG

184
Q

What is an ECoG

A

Intracranial EEG
For research purposes, often paired with some form of stimulation
Must already be having brain surgery

185
Q

What is MEG

A
  • Very similar to EEG, but waves are not distorted by skull
  • Measuring magnetic waves instead of electrical
  • Usually MEG is overlaid on top of high resolution MRI
  • Better spatial resolution
  • But you need to shield out any other magnetic fields including the earth’s magnetic fields and requires liquid helium to cool some of the sensors
  • Only 100 machines in the world and are super expensive
186
Q

What are the two types of Functional Brain Imaging Techniques

A

PET and fMRI

187
Q

How do PET scans work

A

Different radioactive agents can be used with biomarkers of disorders and pathologies
Other types of tracers can be used to assess function such as FDG and oxygen-15
Can label neurotransmitters
Good for task related activations
Brain metabolism and neurochemistry

188
Q

What are the problems with PET scans?

A

Bad spatial resolution
Slower temporal resolution
Injecting people with radioactive isotopes
Doesn’t image brain structure
Nurse must be on site

189
Q

What are MRIs

A

Relies on extremely strong magnets
Non-invasive
High spatial resolution

190
Q

What is an fMRI

A

Indirect measure of neural activity through oxygen levels

Most often measures the blood oxygenation level dependant signal (BOLD)
When neurons fire, they require additional oxygen BOLD relies on the different magnetic properties of oxygenated and deoxygenated blood
Measures ratio of oxygenated to deoxygenated blood to see which areas are active
Increased neural activity → increased blood flow → surplus of oxygenated blood → increased BOLD signal
Break up the brain into smaller voxels (1-3 mm cubes) so each voxel contains roughly 100,000 neurons to see the BOLD signal in multiple voxels
Look at haemodynamic response

191
Q

How does BOLD work?

A

Increased neural activity –> increased blood flow –> surplus of oxygenated blood –> increased BOLD signal

192
Q

What do MRIs show?

A

Brain Structre:
- White and gray matter
- Bone shown but CT is better for this
- Cortical thickness (distance between gray matter and white matter)

193
Q

Why are MRIs good

A

non-invasive and high spatial resolution

194
Q

Down-regulation definition

A

The state one is in during depression and BDNF helps get us out of it

195
Q

Where does the Mesolimbic pathway start and end? And what is the dominant neurotransmitter?

A

VTA –> Ventral Striatum and Dopamine

196
Q

Are benzodiazpines and alcohol GABA agonists or antagonists

A

GABA Agonists

197
Q
A

Biopsychology (2 decks)

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