Unit 5 Flashcards

1
Q

Attention

A
  • Selective focus on one aspect of sensory input, while filtering out other stimuli
  • Bottom-up and top-down attentional processes compete
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2
Q

Bottom-Up Attention

A
  • A stimulus demands attention
  • Ex: sudden movement in visual field, smell of gas, hearing the phone right
  • Sensation–> Perception–>Interpretation–> Evaluation–> Expectation–> Prediction
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3
Q

Top-Down Attention

A
  • You purposefully direct your focus to a stimulus or task
  • Ex: Attend to your textbook instead of roommates talking, search for a specific shape of a puzzle piece
  • Prediction–> expectation–> evaluation–> interpretation–> perception–> sensation
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4
Q

How does attention increase task performance?

A

Accelerates..

  • Sensory Processing
  • Decision making
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5
Q

How is attention detected neurally?

A

-fMRI can compare brain activity (BOLD response) in specific regions in response to specific attentional tasks
-Compared to “resting state”
–Not absense of activity, just default mode network
Brain region depends on: task, sensory modality, specific stimuli, employment of top down

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6
Q

Default Mode Network

A
  • Brain regions active at rest are consistent across individuals
  • These active regions decrease activity when task is being performed
  • Medial prefrontal cortex and posterior cingulate cortex show coordinated activity at rest
  • Other regions: posterior parietal cortex, hippocampus, lateral temporal cortex, amygdala
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7
Q

What does the default mode network do?

A
  • Does not process sensory input
    1. Sentinel hypothesis:
  • Constantly on the lookout for stimuli
  • Depends on peripheral vision, not focus
    2. Internal mentation hypothesis:
  • medial prefrontal cortex, posterior cingulate cortex activated when remembering past event or thinking of future event
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8
Q

Common Attention Tasks

A
  • Directed shifts in attention to different stimuli
  • -Response may be monitored to confirm attention/motivation
  • Complete a task while being presented w/ distractors
  • -Responses may be monitored to see effects on accurate performance
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9
Q

Brain and Multitasking

A
  • Brain can easily and quickly shift btwn tasks, but cannot multitask
  • -Especially when tasks rely on diff sensory modalities
  • Errors increase when multitasking
  • Time to complete tasks doubles
  • Reduced recollection
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10
Q

Salience Map

A
  • Top-down input refines feature combos of stimuli

- Attention directed to most salient stimuli (what image to focus on)

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11
Q

Fronto-Parietal Attention Network

A
  • Attentional Pathway
  • —Bottom-up attention
  • ——-stimulus directs attention to eye movement
  • —Top-down attention
  • ——-Eye movement used to shift attention
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12
Q

Bottom-Up Processing for Multisensory Input and attention

A
  • Pairing sensory stimuli demands greater attention

- –Ex: hearing a crash and seeing a moving vehicle come to a stop

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13
Q

Top-Down processing of multisensory input and attention

A

-Attention of several modalities simultaneously (limited)

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14
Q

Conciousness

A
  • The awareness of specific stimuli
  • Concepts associated:
  • –Self-conciousness, self-awareness, awareness, concious of stimuli, attention, concious states wakefulness
  • Awareness of specific stimuli= attention
  • No waking versus sleeping, instead diff states of conciousness
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15
Q

Reductionism

A
  • Method to study conciousness
  • In search of the neural correlates of consciousness
  • Individual parts summing up the whole
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16
Q

Holism

A

-Something about entire being leads to conciousness

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17
Q

Emergence

A

-Synergisitic effects add up to phenomenon of conciousness

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18
Q

Dualism

A

-Something totally separate from body that explains conciousness

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19
Q

Binocular Rivalry Experiments

A
  • The brain can only “see” one percept at a time
  • -Takes advantage of this
  • Mokey trained to pull left lever w/ starburst, right for face
  • Measure single neuron activity in inferotemporal cortex (Object ID)
  • Showed impages to diff eyes
  • Neuronal activity level corresponding w/ stimuli observed w/ associated lever pull
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20
Q

3D Glasses experiment

A
  • Glasses determine which eye sees which image (house or face)
  • If see house then face, increased activity in PPA, folowed by increased in FFA
  • If see face then house, increased activity in FFA, folowed by increase in PPA
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21
Q

Neurpsychiatric Disorders

A
  • Genes and environment both play role in neurodevelopment
  • Common risk factors manifest differently in different individuals
  • Difficult to treat disorders bcuz poor understanding of risk factors and how to intervene
  • High contribution to disease burden
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22
Q

How are disorders studied?

A
  • DSM-5 has signs and symptoms
  • Neuropsych. assessments
  • Neuroimaging
  • Biomarkers
  • In order to diagnos, must exclude other disorders
  • -Informs treatment options
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23
Q

How is etiology studied?

A
  • Environment
  • Pathology
  • Genetics
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24
Q

Multipule Hit Hypothesis

A
  • Genes have lifelong developmental effects
  • Environmental insults (infection, toxins) and exposure to trauma (stress, isolation) have developmental effects later in life
  • Lead to neurotransmitter dysfunction/imbalance, neurocircuitry dysregulation, structural abnormalities
  • Spectra of symptoms/severity
  • *Treatment focuses on symptoms
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25
Q

Schizophrenia and Genes

A
  • 80% heritable= portion of trait within pop. attributed to genetics
  • Difficult to identify specific genes w/ strong associations to disorder, although genetic component is proven
  • Complex behavioral traits are controlled by many genes, each with small effects
  • Biomarkers not always reliable
  • -Enlarged ventricles w/ schizophrena
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26
Q

Construct Validity

A
  • The etiology/cause is similar

- Ex: transgenic mouse with mutation that is associated with the human condition

27
Q

Face Validity

A
  • The model ‘looks like’ the disorder (similar symptoms)

- Ex: mouse model of autism spectrum disorder shows lower social approach

28
Q

Predictive Validity

A
  • The model is responsive to treatments that effectively treat the disorder
  • Ex: rats given anti-depressant drugs decrease time spent immobile in forced swim test
29
Q

Schizophrenia Windows of Vulnerability

A
  • Pre/perinatal
  • Adolescence
  • -When neural development active
30
Q

Positive Symptons of Schizophrenia

A
  • Add onto experience
  • Delusions
  • Hallucinations
  • Disorganized speech
  • Grossly disorganized or catatonic behavior
31
Q

Negative Symptoms of Schizophrenia

A
  • Take away from normal experience
  • Reduced expression of emotion
  • Poverty of speech
  • Difficulty initiating goal-directed behavior
  • Anhedonia-> Loss of pleasure
  • Social behavior deficits
32
Q

Cognitive symptoms in Schizophrenia

A
  • Learning and memory impairment

- Presented early

33
Q

Dopamine Hypothesis of Schizophrenia

A
  • Psychosis triggered by activation of dopamine receptors
  • Ex: high dosage of stimulants leads to this
  • Conventional antipsychotics, act as antagonists at D2 receptors
  • –Reduce the positive symptoms of schizophrenia
  • Side effects= parkinsons symptoms
34
Q

Glutamate Hypothesis of Schizophrenia

A
  • PCP and ketamine lead to behavior affect synapses that use glutamate as a neurotransmitter
  • –Inhibit NMDA receptors

-Diminshed activation of NMDA receptors in the brain
===Increade in mesolimbic DA and decrease in PFC
—Increased DA in NAc related to positive symptoms
—Decreased DA in cortex related to negative symptoms

35
Q

Current Treatments of Schizophrenia

A

Antipsychotics:
–Block D2 receptors= improving positive symptoms
–Antagonists at 5-HT2 receptors= improve neg symptoms
–Target the acetylcholine system= improve cognitive symptoms
Drug therapy combined with psychosocial support

36
Q

Declarative Memory

A
  • Explicit/ “Knowing that”
  • Episodic memory, semantic memory
  • Brain Regions: medial temporal lobe, diencephalon, neocortex)
  • Know facts, events, spacial info, relationships
  • Ex: What is an NMDA receptor
37
Q

Nondeclarative Memory

A
  • Implicit/ “Knowing how”/unconcious
  • Brain Regions: Medial temporal lon, diencephalon, neocortex
  • Classical conditioning (amygdala, cerebellum)
  • skeletal musculature (cerebellum)
  • procedural memory/ skills and habits (basal ganglia)
  • emotional responses (amygdala)
  • habituation, sensitization (sensory/reflex pathways)
  • perceptual learning/priming, recognition memory (neocortex)
  • Ex: Playing the piano
38
Q

Retrograde Amnesia

A

-Cannot recall old memories from before trauma

39
Q

Anterograde Amnesia

A

-Cannot recall memories after trauma

40
Q

Patient HM

A
  • Anterograde amnesia
  • Couldn’t recognize doctor of 50 yrs
  • No effect on intelligence, perception, personality
  • Impaired memory for experience, but spared memories of skills and simple associations
41
Q

Bottom-Up Attention Recruits…

A
  • begins w/ stimuli input, recruits:
  • -LIP–priority map constructed from bottom-up and top-down input
  • -FEF–directs eye movement
42
Q

Top-Down Attention Recruits…

A
  • Begins in Prefrontal cortex (executive control of top down) and recruits
  • -FEF
  • -LIP
43
Q

Sensory Memory

A
  • Vivid, lasts seconds
  • Sensory Cortex
  • “Hearing but not listening”=repeating things said to you a few seconds ago when not listening
44
Q

Short term memory

A
  • Lasts minutes to days
  • Limited in capacity
  • Tends to be abstract
  • Sensory cortex, hippocampus
45
Q

Working Memory

A
  • Mental sketch pad
  • Dorsal prefrontal cortex
  • Tested by N-back test
46
Q

Consolidation

A
  • Bringing info from short-term and working memory into long term memory
  • Depends on sleep, time, protein synthesis
  • Early LTP–> consolidation–> Late LTP
47
Q

Long term memory

A
  • Virtually limitless
  • Most stable
  • Two types: nondeclarative and declarative
48
Q

Hebbs Rule

A
  • Stimulus–> activation of cell assembly (group of neurons that work towards certain memory)
  • —Cells activated at same time to learn memory, connectivity increases w/ increased firing
  • Neurons that fire together, wire together= Long Term Potentiation
  • Neurons that fire appart, wire appart= long term depression
  • *Changes in synaptic strength correspond to changes in EPSP and IPSP magnitude
49
Q

Learning and Memory of Idea

A
  • Learning and memory of idea occurs at synapses
  • Ideas related to idea are strengthend w/ repetion
  • Weakened if not releated to idea/not repeated
50
Q

Neural Network Model

A
  • Memories are constellations of neurons
  • Advantage= memories can survive damage to individual neurons
  • Graceful degradation of memories w/ gradual neuron loss
  • Location for diff types of memory differ
51
Q

Where are cell assemblies found?

A
  • Found in hippocampus (part of the limbic system)
  • —In rat: caudal telencephalon
  • —In humans: temporal lobe
  • —Dentate gyrus nesseled in between hippocampus
52
Q

Sensory info pathway

A

Sensory info–> cortical association areas–> parahippocampal and rhinal cortical areas–> hipocampus–fornix–> thalamus, hypothalamus

53
Q

Long Term Potentiation in Rats

A
  • Rat restricted to light side of box
  • Dark side opened and rat explored–> shock
  • Rat learns not to go to dark side of box
  • LTP to avoiding dark side
54
Q

Long Term Potentiation

A
  • Strengthening of a cell assembly
  • Strong depolarization of postsynaptic neuron
  • Input 1 and Ca1 neurons fire together
55
Q

Long Term Depression

A
  • Weakening of cell assemly
  • When post synaptic cell is weakly depolarized by other inputs, active synapses undergo LTD
  • -Input 1 and Ca1 neurons fire appart
56
Q

Glutamate receptors and LTP

A
  • NMDA and AMPA= ionotripic receptors

- Found on dendritic spines of excitatory projection neurons

57
Q

Step 1 of glutamate receptors in LTP

A
  • Glu released; Binds to AMPA and NMDA receptors

- -NMDA receptor blocked by Mg2+; AMPA conducts Na+

58
Q

Step 2 of glutamate receptors in LTP

A
  • AMPA receptors depolarize membrane

- -NMDA receptors conduct Ca2+ (Mg2+ released from pore)

59
Q

Step 3 of glutamate receptors in LTP

A
  • Ca2+ causes activation of CaMII, Protein Kinase A and C

- –activates proteins necessary to establish LTP

60
Q

What is a kinase?

A

-An enzyme that adds a phosphate group to other receptors to activate them

61
Q

How Hebbs Relates to LTP and LTD

A
  • When NDMA receptors are opened:
  • –Glutamate–> firing of Ca3
  • –Depolarization–> Ca1 fires
62
Q

Step 4 of glutamate receptors and LTP

A
  • Kinases catalyze synaptic plasticity
  • –Exocytosis of more AMPA receptors to synaptic membrane
  • –Increased conductance of AMPA receptors (greater depolarizations/EPSPs)
63
Q

Step 5 of Glutamate receptors and LTP

A
  • Consolidation (Late LTP)
  • Kinases activate (phosphorylate) transcription factors and epigenetic markers
  • IF THIS STEP DID NOT HAPPEN MEMORIES WOULD BE ERASED*