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Neuro > Neuro mod 3 > Flashcards

Neuro mod 3 Flashcards

1
Q

process of acquiring new info, behavior patterns or abilities , characterized by modifications of behavior as a result of practice, study, or experience
-systemic relatively permanent change in behavior that occurs through experience
*dependent on ability to take in info from outside & process it

A

learning

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2
Q

ability to retain info based on mental process of
1. learning of ENCODING
2. RETENTION across some internal of time
3. RETRIEVAL or reactivation of the memory

A

memory

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3
Q

very brief stores sensory impression of scene

A

iconic memory

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4
Q

form of memory that usually lasts a dew seconds as long as its rehearsed
-closely tied to working memory –> holding information in mind

A

short-term memory

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5
Q

a form of memory that outlasts short term memory (STM) but not LTM

A

intermediate memory

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6
Q

enduring form of memory that lasts days, weeks, years

includes:
-episodic
-declarative
-nondeclarative

A

long term memory

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7
Q

-knowledge about world – FACTS anyone can know
-info about an area of expertise
-general knowledge
things learned in school
*I KNOW

A

semantic memory

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8
Q

-info is autobiographical
-the what where when & how
-*I REMEMBER
ex. fav halloween, losing 1st tooth, etc.

A

episodic memory

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9
Q

info is verbally communicated that helps you remember

A

declarative/explicit memory

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10
Q

things you know by doing it

A

non declarative (implicit) memory

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11
Q

learning to perform a task that requires motor coordination
-form of non declarative memory

A

procedural memory (skills)

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12
Q

phenomenon by which exposure to a stimulus facilitates a subsequent response to the same or similar stimulus

-change in how you process stimulus based on the prior exposure to same stimulus or similar stimulus

A

priming

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13
Q

form of learning by which an organism comes to associate 2 stimulus & a response

A

classical conditioning

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14
Q

-severe seizures
-got rid of hippocampus
-partial retrograde amnesia
-complete anterograde amnestia
-can do STM tasks
-can form implicit memories

He could:
-digit span –> succeed if allowed to rehearse (shows he has STM)
-recall early life events
mirror drawing test –> couldn’t remember task but got better
-eye blinking conditioning

A

H.M.

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15
Q

-novel stimuli
-emotional stimuli
-large objects
-vividly colored objects
-things moving

A

Encoding
-attentional processes
likely to remember these things

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16
Q

noting physical features of a stimulus

A

shallow

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17
Q

giving the stimulus a label

A

intermediate

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18
Q

thinking about the meaning of the stimulus

A

deep

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19
Q

memory system that holds info temporarily as we perform cognitive tasks
*caudate nucleus –important for retaining a motor response
*visual cortex – important for recognition of objects/visual stimuli
*hippocampus – important for spatial recognition (location)

A

working memory

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20
Q

important for recognition of objects/visual stimuli

A

visual cortex

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21
Q

important for spatial recognition (location)

A

hippocampus

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22
Q

important for retaining a motor response

A

caudate nucleus

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23
Q

-try to remember if you saw something before
-activation in the left hemisphere frontal cortices
-rehearsal of info via the phonological loop

A

N-back task

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24
Q

-binding of info occurs in __ ~3 days then ,over to frontal regions
-memories are temporally stored in the ___ but shift to cortical areas for long term memory storage

A

importance of hippocampus

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25
Q

memory widely distributed but different loci store different aspects of while

A

connectionism

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26
Q

what lobe is important for episodic storage

A

anterior frontal lobe

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27
Q

what lobe is important for semantic storage

A

-posterior frontal lobe
-temporal lobe

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28
Q

-stem completion task
-priming based on visual word form
-reduced activation in the occipitotemportal cortex

A

perceptual priming

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29
Q

-false memory task
-priming based on word meaning
-reduced activation in left frontal cortex

A

conceptual priming

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30
Q

involved in planning + problem solving
*rely based on ganglia

A

skill memory

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31
Q
  • involves the encoding of relationships between events, for example, between two stimuli or between a stimulus and a response
    -cerebellum
    -activation increase in hippocampus
A

associative learning

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32
Q

hippocampus + cortex b/c needed for declarative memory

A

complex association

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33
Q

stable + enduring increase in effectiveness of synapses following repeated, strong stimulation
possible mechanism for learning + memory at neuronal level

Can occur:
invertebrates + vertebrates
-many brain regions

A

long term potentiation

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34
Q

-synaptic connections stronger and more effective

A

Bliss + Lomo

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35
Q
  1. NTs (glutamate – important for learning and memory) released from presynaptic neuron
  2. NTs bind to receptors on postsynaptic neuron
  3. affect channels (AMPA & NMDA) on postsynaptic membrane
A

LTP occurring early stages

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36
Q
  1. glutamate binds to NMDA & AMPA receptors
  2. AMPA channels open, Na+ comes into cells
    -NMDA receptors blocked by Mg2+ –> voltage dependent + needs increased depolarization to remove block otherwise no LTP
  3. Mg2+ removed with sufficient depolarization
  4. once Mg2+ removed –> Na + Ca –> postsynaptic neuron
  5. Ca2+ activates CAMKII (protein kinase that alters or activates other proteins)
  6. CAMII
    - adds AMPA Chanels into neuron membrane –> causes nearby AMPA channels to move to synapse –> increases conductance of NA+
    *ADDED AMPA CHANNELS –> glutamate can bind to postsynaptic neuron
    *increase singling ability
    *lasts 1-3 hours
  7. along with CAMKII Ca2+ activates other protein kinases
  8. these kinases act on CREB (transcription factor – binds to promotor region – change in gene expression)
  9. CREB tells neuron to make: (kinases, receptors, & dendrites)
A

specifics of late LTP

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37
Q
  1. new synaptic connections
  2. greater signaling ability btw existing neuronal connections
  3. reshaping of neuron
    *renders LTP relatively permanent
A

late LTP gene transcription effects

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38
Q

-retrograde messengers released from postsynaptic cell
-signal presynaptic cell to release more NT

A

effects of presynaptic neuron

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39
Q
  1. threshold dependency: LTP can happen if neuron has repetitive stimulation –> allows is to learn form repetitive info
  2. Input specificity: only want to make connections between pieces of info that should be connected
    - LTP doesn’t affect neighboring synapses that aren’t active
  3. associativity: do want association of certain info (ex. classical conditioning)
    -if neighboring pathway is being strongly stimulated, both synaptic pathway undergo LTP
A

properties of LTP

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40
Q

process by which specific sets of synopsis are selectively weakened
-low level activation for extended time
-smaller EPSP

A

long term depression

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41
Q
  1. glutamate binds to NMDA + AMPA receptors
  2. AMPA channels open Na+ in cell
  3. Mg2+ remove with sufficient depolarization (-35 mv)
  4. once mg2+ is removed Na+ + Ca2+ –> postsynaptic neuron
  5. Ca2+ activates calcineurin
    -protein phosphates alter other proteins + removes phosphate groups
  6. calcineurin activates protein phosphates (PP1)
  7. calcineurin & PP1 act on AMPA receptors in membrane to remove them
    *calcunerurin has higher affinity for ca than CAMKII
    *amt of CA2+ determines LTD or LTP occurring
A

specifics of LTD

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42
Q

dendrites shrink or disappear
-process complex: some signaling may rely on proapoptic mechanisms

A

specific of LTD

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43
Q

brings together biological, psychological, and sociocultural features to understand abnormal behavior

A

biopsychosocial model

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44
Q

-most common psychosis: severe mental disorder
-broad spectrum of cognitive + emotional dysfunction
-can disrupt perception, thoughts, speech, & movement
-diagnosis based on behavioral symptoms

A

schizophrenia

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45
Q

system of beliefs that would be seen by most members of the society as misrepresentations of reality
-grandeur + persecutions
*FALSE BELIEFS

A

delusions

46
Q

experience of sensory events without any inout from surrounding environment
-auditory ____ is most common

A

hallucinations

47
Q

erratic speech

A

disorganized speech

48
Q

erratic motor behavior + emotional reactions
-catatonia: waxy effect

A

gross disorganized or catanoic behavior

49
Q

-emotional + social withdrawal
-apathy
poverty of thought/speech

A

negative symptoms of schizophrenia

50
Q

-delusions
-hallucinations
-disorganized speech

A

must have 2+ symptoms during 1 month period to be diagnosed with schizophrenia

51
Q

-large ventricles –> atrophy or damage to brain areas bordering ventricles
-neuronal inputs + outputs are disorganized
Smaller:
-hippocampus
-amygdala
-entorhinal cortices
-hippocampus
-cingulate cortex
-prefrontal cortex

A

structural differences in SZ

52
Q

less metabolic activity during difficult cognitive task
-function difference in SZ

A

hypofrontality hypothesis

53
Q

What causes differences in psychopathology

A

-genetic + environmental factors
-likely gene-environment interactions –> epigenetic effects

54
Q

-genes responsible for making some individuals vulnerable to SZ
-children w/ biological parents w/ SZ –> increase of SZ
-If MZ twin w/ SZ –> -48% chance
-DZ twin w/ SZ –> 17%

SNPS
-regulate expression of genes upstream or downstream of loci
-impact non-protein coding genes

A

Genetic vulnerability for SZ

55
Q

-whether particular genes associated with particular traits
-SNPS + SZ
*no confirmed casual mutations underlying SZ

A

genome wide association studies

56
Q

-monozygotic
-onset, symptom diagnoses, disorder, outcomes differ

A

case of genuine quadruplets

57
Q

dopamine system too active (hyperdopaminergic) in individuals diagnosed w/ SZ
-not an issues w/ clearance at synapse
-not issue of too many D2 receptors
-more tyrosine hyroxylase –> D2

Evidence
-Amphetamine use
-treat with resperine
-treat Parkinson w/ L-Dopa

A

dopamine hypothesis

58
Q

leads to increase conc. of DA –> increase psychotic symptoms

A

amphetamine use

59
Q

decrease extracellular concentration of DA –> no psychotic symptoms

-deletion of monoamines = depressive symptoms
-deletion of tryptophan (precursor for 5-HT) –> depressive symptoms

A

resperine

60
Q

-antagonists at D2 receptor –> lack of effect + NTs can’t act
-to be effective, drug must bond optimal # of D2 receptors
-<50% – little to no response
-75% – risk off extrapyramidal side effects increase
- > 50% – increase response

A

antipsychotic

61
Q

DA plays role in assigning motivational salience to internal or external stimuli. In this swat DA determines which stimuli grab our attention + drive behavior

A

abberent salience model

62
Q
  1. elevation of DA –> release in absence of appropriate stimuli
  2. dysregulated release leads individuals to attribute salience to irrelevant stimuli
  3. everyday occurrences imbued w/ sense of inexplicable significance
  4. individuals build delusion based around these occurrences
A

relation of DA dysregulation + symptoms

63
Q
  1. DA dysregulation
  2. increase “noise” in system & drowning out DA signals linked + reward
  3. reduction in motivation drive
  4. social withdrawal + neglect of interest
A

negative symptoms of SZ

64
Q

-1/3 patients don’t show or late response to increase D2 receptors occupancy
- too much DA in striation
-not enough DA in prefrontal cortex
-suggest more than just DA system involved

A

problems w/ DA hypothesis

65
Q

-interaction btw DA & Glu systems
-NMDA antagonists can influence DA synthesis + firing patterns

A

glutamate disorder

66
Q

psychological primary disturbance of mood
-fundamental experiences of depression + mania contribute to mood disorders

A

mood disorder

67
Q

-most commonly diagnosed depressed
-most severe depression
*symptoms must persist for at least 2 week
-characterized by physical changed + emotional shutdown = +/- sleep
*too little monoamines
treatments: MADIS, TCA, SSRIs, + CBI

symptoms:
*reduced interest or pleasure in all or most activities: anhedonia
-physical changes
-behavioral/emotional shutdown

A

Major Depressive Disorder

68
Q

-size reduction in limbic + cortical structures:
-hippocampus
-obitofrontal cortex
-sub-genual prefrontal cortex
-episodes longer + multiple related relapses

amygdala sizes vary
-enlarges onset and reduced as progressed
-move pronounced reduction in women

A

structural differences in MDD

69
Q

-hyper activation of HA axis: feedback loop for responding to stress
-potential role in volumetric changes in hippocampus, OFC, PFC, & amygdala
-mood congruent emotion processing bias: hypersensitive to negative stimuli & hypostimuli to positive stimuli
-lack of ability to regulate negative emotion
– less activation in dorsolateral prefrontal cortex
–involved in emotion regulation + executive control

A

Functional differences in MDD

70
Q

-2-3x more likely to have depression if fam member has been diagnosed
Mz: 60% DZ: 20.2%
adoption: increase likelihood of developing depression of biological parent diagnosed

A

genetic factors of MDD

71
Q

most strongly associated with occurrences of MDD – involve ed in the circadian rhythm

A

RRA gene

72
Q

-low SES (socioeconomic status)
-minority women
-situational factors
-minority women
-dysregulation of NT: monoamine hypothesis (NDR, DA, H-5A

A

environmental factors for MDD

73
Q

food with increase tryptophan – can’t break down in gut –> hypertensive crisis + dietary restrictions

A

effects of MAOI

74
Q

increase monoamines = no depressive symptoms

A

TCA effects

75
Q

MAOI break down monoamines
-antipsychotic

-MAOIs block the action of MAOs degradation of monoamines

A

iproniazid (MAOI)

76
Q

tricyclic antidepressant (TCA)
-block reuptake of 5-HT + NE –> evidence of monoamine dysregulation
-antipsychotic

-increase monoamines = no depressive symptoms

A

imipramine (TCA)

77
Q

-main drug to treat depression
-more selective in how they act MAOIs or TCAs
-fast acting
-help in stages
1. normal action of autoreceptors –> decrease 5-ht release at synapse
2. when SSRIs act autoreceptors over activated –> also down signal –> slow down 5-HT release
3. autoreceptors become desensitized after few weeks –> increase signaling

effects:
-50% decrease in firing rate
-ventral tegmental area normally fires in response to neurons –> decreased in patients on SSRIs
-decrease in response to chocolate
-decrease in reward processing

A

development of SSRI (selective serotonin reuptake inhibitors)

78
Q

1/3 of patients don’t respond to treatment

A

problems with monoamine hypothesis

79
Q

-reshape interpretation of life (what kind of therapy?)
-often used in combo with antidepressant –> increase improvement
-kind of thoughts + beliefs you have about situations contributing to hopelessness

A

cognitive behavioral therapy

80
Q

involves fears that are uncontrollable, disproportionate to actual danger that person might be in & disruptive to ordinary life

A

anxiety disorder

81
Q

negative mood state characterized by bodily symptoms of physical tension by apprehension about FUTURE

A

anxiety

82
Q

-2-5% of pop meets criteria for GAP during 1 year period
-6% at some point during lifetime
-most common anxiety disorder
-2/3 women – changes by culture
*marked by persistent anxiety for at least 6 months
*individuals unable not specify source of anxiety
*TREATMENTS –> BZI

A

GAD

83
Q

-interest in amygdala – fear circuit region
-increase gray matter
-prefrontal cortex larger
-reduction in hippocampus
-increase functional manners for FAD than structural `

A

structural differences in GAD

84
Q

-decrease connectivity btw amygdala + PFC
-decrease connectivity btw amygdala & anterior angulate cortex (ACC)
-increase activation of PFC when presented with worry statements
-increase activation of FFC when presented with worry statements

A

functional differences in GAD

85
Q

-genetic + environment
-NT dysfunction

A

what causes these structural and functional differences in GAD patients

86
Q

15% of people with relatives diagnosed with GAD also have GAD
twins
MZ: 21.5%
DZ: 12.5%
-genome wide association studies

A

genetic factors of GAD

87
Q

perceive world as dangerous/out of control
-life stressors

A

environmental factors of GAD

88
Q

lacks ability to inhibit worry/anxious feelings

A

NT dysregualtion hypothesis

89
Q

-act on GABA signaling system
-GABA is mainly inhibiting NT in CNS
*increase concentration of GABA receptors in cortex & limbic system
-decrease excitability of neurons + produces calming effect on brain
-positive (agonist) allosteric (indirect) modulator at receptor site
-GABA receptor complex has 5 subunits
-2 GABA binding sites
-1 BZD binding site
-BZD binding –> changing receptor confirmation –> increase in GABA affinity

BZD action
-modulates binding of GABA
-increase cloning coming into neuron –> IPSP

A

benzodiazepines (BZD)

90
Q

-stop taking –> anxiety returns
-take in large doses = physical dependence

bad side effects:
-depression
-memory loss
-aggressive behavior
-lack of coordination
-interacts with other substances ex. alcohol
*good for short term
*only take for ~1-2 weeks

A

problems with BZD

91
Q

-anxiolytic –> developed as antipsychotic
-approved for GAD
-5HT partial agonist
-g couple protein –> inhibiting effects

A

Buspirone

92
Q

system of advantaged based on race that is created and maintained by an interplay btw psychological factors + sociopolitical factors
*race meaningful by 9 yo

A

racism

93
Q

-a collectokin of individuals who have at least 1 attribute in common but otherwise doesn’t necessarily interact
-used to conceptualize in groups + out groups
-preferring “like me” starts early

A

social category

94
Q

mere exposure to people form a group increase liking for characteristic of that group

A

familiarity (contact) hypothesis

95
Q

taught explicitly or implicitly to attend race as meaningful category

A

minimal group hypothesis

96
Q

groups can be formed cause of?

A

-group labels
-visual markers of groups (ex. t-shirts)
*type of language used – using as an individual or group?

97
Q

leads children to infer proteins applies to ALL category members
-sterotypes can be passed across genetic by parents ‘likelihood’ of generic language

A

generic language

98
Q

any state of mind, feeling , or behavior that criticizes others on account of social group to which they may belong to

A

prejudice

99
Q

widely held belief about a group

A

stereotyping

100
Q

unjust or prejudicial treatment of different cauterizes of people

A

discrimination

101
Q

-measures strength of association between concepts, evaluations, or sterotypes
-participants sort words or images into categories
-if have implicit bias tp associate white with w=good and black with bad, it’ll take longer to respond to stereotype incongruent trials
*strength of bias reflected in difference in RT btw those types

A

implicit bias test (IAT)

102
Q

Hierarchal control model:
Stage 1: low level (mostly) automatic processing
-detects categorizes, evaluates race

Stage 2: higher order processing
-exert control over bias reactions
-achieve personal + societal goal of combating racism

A

Processing someone’s race

103
Q

-fusiform gyrus located in ventral occioototemporal cortex –> Fusiform face area (FFA)
-sensitive to faces
-increase activation to in-group than outgrip faces in FFA
*enhanced processing in group members

A

face encoding

104
Q

posterior cingulate PCC
-activated when retrieve info about PEOPLE WE KNOW
-increase activation to strangers in in-group than outgroup

A

posterior knowledge

105
Q

-representation of social knowledge
-acitvation when categorizing based on stereotype relevant judgement
-lots of connections to VMPFC

A

anterior temporal lobe

106
Q

-social information processing
-sensitive to humanness
-theory of mind takes
-lack of VMPFC activation = dehumanization

A

vental medial PFC

107
Q

amygdala: almond shaped structure in medial temporal lobe, part of limbic system
-emotional learning + memory
do you feel a threat?

increase activation when:
-direct eye gaze
-judgement made in context of threat
-presentation is brief
*amygdala activation reflects more than processing of perceptual features

ERPs: show preaches of race in 1/10 of sec
increase amplitude for out group members
-greater response = vigilant attention to potential threat
-increase effect in those with stronger implicit prejudice

A

amygdala

108
Q

make decisions based on center item, ignoring other items
*longer response times on incongruent trials

A

flanker task

109
Q

-*MONITORS FOR RACIAL BIASES
-monitors for conflicts in automatic + intentional responses
-when conflicts occur, executrices control is engaged
*monitor what is going on
-event related negativity (ERNS) is an ERP response widely associated with ACC engagement
-individual internally motivated to non-prejudice show increase ERNS when stereotype incongruent error on stoop like tasks

A

anterior cingulate cortex

110
Q

-regulating racial biases
-top down control of sensory + motor representation activation in working memory
-cognitive regulation of emotions can modulate amygdala response
-may be engages to inhibit implicit race attitudes during interactions with racial outgroup members

A

dorsal lateral prefrontal cortex (DLPFC)

Neuro (9 decks)

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